query: part of the adrenal gland that secretes epinephrine and norepinephrine

pos: Adrenal medulla Adrenal medulla The adrenal medulla () is part of the adrenal gland. It is located at the center of the gland, being surrounded by the adrenal cortex. It is the innermost part of the adrenal gland, consisting of cells that secrete epinephrine (adrenaline), norepinephrine (noradrenaline), and a small amount of dopamine in response to stimulation by sympathetic preganglionic neurons. The adrenal medulla consists of irregularly shaped cells grouped around blood vessels. These cells are intimately connected with the sympathetic division of the autonomic nervous system (ANS). In fact, these adrenal medullary cells are modified postganglionic neurons, and preganglionic autonomic nerve

pos: Adrenal medulla compensation by the autonomous nervous system, except in episodes of hypoglycemia where glycogenolysis cannot be stimulated by circulating epinephrine . In dopamine beta hydroxylase deficiency, the entire body cannot efficiently produce epinephrine and norepinephrine from dopamine, this results in severe dysautonomia but most crucially due to autonomous nervous system failure which requires epinephrine and norepinephrine as neurotransmitters, dopamine being used in this pathology as an inadequate substitute. Adrenal medulla The adrenal medulla () is part of the adrenal gland. It is located at the center of the gland, being surrounded by the adrenal cortex. It is the innermost part of

pos: Adrenal medulla Adrenal medulla The adrenal medulla () is part of the adrenal gland. It is located at the center of the gland, being surrounded by the adrenal cortex. It is the innermost part of the adrenal gland, consisting of cells that secrete epinephrine (adrenaline), norepinephrine (noradrenaline), and a small amount of dopamine in response to stimulation by sympathetic preganglionic neurons. The adrenal medulla consists of irregularly shaped cells grouped around blood vessels. These cells are intimately connected with the sympathetic division of the autonomic nervous system (ANS). In fact, these adrenal medullary cells are modified postganglionic neurons, and preganglionic autonomic nerve

pos: Adrenal gland disorder adrenal medulla produces epinephrine (adrenaline) and norepinephrine (noradrenaline). Disorders of the adrenal gland may affect the production of one or more of these hormones. Adrenal gland disorder Adrenal gland disorders (or diseases) are conditions that interfere with the normal functioning of the adrenal glands. Adrenal disorders may cause hyperfunction or hypofunction, and may be congenital or acquired. The adrenal gland produces hormones that affects growth, development and stress, and also helps to regulate kidney function. There are two parts of the adrenal glands, the adrenal cortex and the adrenal medulla. The adrenal cortex produces mineralocorticoids, which regulate salt and water

pos: Adrenaline the adrenal medulla from the amino acids phenylalanine and tyrosine. Epinephrine is synthesized in the medulla of the adrenal gland in an enzymatic pathway that converts the amino acid tyrosine into a series of intermediates and, ultimately, epinephrine. Tyrosine is first oxidized to -DOPA, which is subsequently decarboxylated to give dopamine. Dopamine is then converted to norepinephrine by dopamine beta-hydroxylase. The final step in epinephrine biosynthesis is the methylation of the primary amine of norepinephrine. This reaction is catalyzed by the enzyme phenylethanolamine "N"-methyltransferase (PNMT) which utilizes "S"-adenosyl methionine (SAMe) as the methyl donor. While PNMT is found primarily in

pos: Adrenal gland catecholamines adrenaline and noradrenaline, released by the medulla. Approximately 20% noradrenaline (norepinephrine) and 80% adrenaline (epinephrine) are secreted here. The adrenal medulla is driven by the sympathetic nervous system via preganglionic fibers originating in the thoracic spinal cord, from vertebrae T5–T11. Because it is innervated by preganglionic nerve fibers, the adrenal medulla can be considered as a specialized sympathetic ganglion. Unlike other sympathetic ganglia, however, the adrenal medulla lacks distinct synapses and releases its secretions directly into the blood. The adrenal glands have one of the greatest blood supply rates per gram of tissue of any organ: up to 60

pos: Sympathoadrenal system pathways that couple with bodily responses to the environment. During numerous diseased states, such as hypoglycemia or even stress, the body’s metabolic processes are skewed. The sympathoadrenal system works to return the body to homeostasis through the activation or inactivation of the adrenal gland. However, more severe disorders of the sympathoadrenal system such as phaeochromocytoma (a tumor on the adrenal medulla) can affect the body’s ability to maintain a homeostatic state. In such cases, curative agents such as adrenergic agonists and antagonists are used to modify epinephrine and norepinephrine levels released by the adrenal medulla. The normal function of the

pos: Sympathoadrenal system in the body. The mechanism lies in epinephrine being secreted by the adrenal medulla and activating glycogenolysis (the break down of glycogen into glucose, or promoting gluconeogenesis (glucose formation). While epinephrine has a greater affect in glucose production, norepinephrine can also increase glucose levels but at high concentrations. It has even been found that norepinephrine may play a role in enhancing the uptake of glucose in skeletal muscle and adipose tissues. As for fat metabolism, the catecholamines (epinephrine and norepinephrine) help stimulate lipolysis (the breakdown of fat) resulting in an increase in energy and a decrease in fat. This explains

pos: Norepinephrine psychiatric drugs exert strong effects on noradrenaline systems in the brain, resulting in side-effects that may be helpful or harmful. Norepinephrine is a catecholamine and a phenethylamine. Its structure differs from that of epinephrine only in that epinephrine has a methyl group attached to its nitrogen, whereas the methyl group is replaced by a hydrogen atom in norepinephrine. The prefix "nor-" is derived as an abbreviation of the word "normal", used to indicate a demethylated compound. Norepinephrine is synthesized from the amino acid tyrosine by a series of enzymatic steps in the adrenal medulla and postganglionic neurons of the sympathetic

pos: Heart rate can impact on this. These include hormones, notably epinephrine, norepinephrine, and thyroid hormones; levels of various ions including calcium, potassium, and sodium; body temperature; hypoxia; and pH balance. The catecholamines, epinephrine and norepinephrine, secreted by the adrenal medulla form one component of the extended fight-or-flight mechanism. The other component is sympathetic stimulation. Epinephrine and norepinephrine have similar effects: binding to the beta-1 adrenergic receptors, and opening sodium and calcium ion chemical- or ligand-gated channels. The rate of depolarization is increased by this additional influx of positively charged ions, so the threshold is reached more quickly and the period of repolarization

pos: Nicotine in some individuals. Chronic nicotine use inhibits class I and II histone deacetylases in the striatum, where this effect plays a role in nicotine addiction. Nicotine also activates the sympathetic nervous system, acting via splanchnic nerves to the adrenal medulla, stimulating the release of epinephrine. Acetylcholine released by preganglionic sympathetic fibers of these nerves acts on nicotinic acetylcholine receptors, causing the release of epinephrine (and norepinephrine) into the bloodstream. By binding to ganglion type nicotinic receptors in the adrenal medulla, nicotine increases flow of adrenaline (epinephrine), a stimulating hormone and neurotransmitter. By binding to the receptors, it causes cell depolarization

pos: Secondary hypertension are also a well known cause of secondary hypertension. Pheochromocytoma (most often located in the adrenal medulla) increases secretion of catecholamines such as epinephrine and norepinephrine, causing excessive stimulation of adrenergic receptors, which results in peripheral vasoconstriction and cardiac stimulation. This diagnosis is confirmed by demonstrating increased urinary excretion of epinephrine and norepinephrine and/or their metabolites (vanillylmandelic acid). Certain medications, including NSAIDs (Motrin/Ibuprofen) and steroids can cause hypertension. Other medications include extrogens (such as those found in oral contraceptives with high estrogenic activity), certain antidepressants (such as venlafaxine), buspirone, carbamazepine, bromocriptine, clozapine, and cyclosporine. High blood pressure that is associated

pos: Adrenaline A general increase in sympathetic neural activity is usually accompanied by increased adrenaline secretion, but there is selectivity during hypoxia and hypoglycaemia, when the ratio of adrenaline to noradrenaline is considerably increased. Therefore, there must be some autonomy of the adrenal medulla from the rest of the sympathetic system. Myocardial infarction is associated with high levels of circulating epinephrine and norepinephrine, particularly in cardiogenic shock. Benign familial tremor (BFT) is responsive to peripheral β adrenergic blockers and β-stimulation is known to cause tremor. Patients with BFT were found to have increased plasma epinephrine, but not norepinephrine. Low, or absent, concentrations

pos: Chromaffin cell parasympathetic paragangliomas of glomus cells). Sometimes only neoplasms of adrenal origin are named pheochromocytomas, while others are named extra-adrenal paragangliomas. Following heart failure, the body increases sympathetic activity to the adrenal medulla as the compensatory mechanism to increase heart rate and cardiac output. This increased sympathetic activity leads to chronically increased synthesis and secretion of catecholamines from the adrenal chromaffin cells. This chronic increase of epinephrine and norepinephrine secretion causes desensitization of the chromaffin cells to catecholamines resulting in a decrease in production and presence of α adrenergic receptors on their cell membrane. This desensitization and downregulation of α adrenergic

pos: Adrenal medulla form clusters around large blood vessels. As a cluster of neuron cell bodies, the adrenal medulla is considered a "ganglion" of the sympathetic nervous system. Rather than releasing a neurotransmitter, the cells of the adrenal medulla secrete hormones. The adrenal medulla is the principal site of the conversion of the amino acid tyrosine into the catecholamines; epinephrine, norepinephrine, and dopamine. Because the ANS, specifically the sympathetic division, exerts direct control over the chromaffin cells the hormone release can occur rather quickly. In response to stressors such as exercise or imminent danger, medullary cells release the catecholamines adrenaline and noradrenaline into

pos: Catecholamine adrenal medulla of the adrenal glands is part of the fight-or-flight response. Tyrosine is created from phenylalanine by hydroxylation by the enzyme phenylalanine hydroxylase. Tyrosine is also ingested directly from dietary protein. Catecholamine-secreting cells use several reactions to convert tyrosine serially to L-DOPA and then to dopamine. Depending on the cell type, dopamine may be further converted to norepinephrine or even further converted to epinephrine. Various stimulant drugs (e.g., a number of substituted amphetamines) are catecholamine analogues. Catecholamines have the distinct structure of a benzene ring with two hydroxyl groups, an intermediate ethyl chain, and a terminal amine group. Phenylethanolamines

pos: John Jacob Abel the position of chair of the department until he retired at the age of 75 in 1932. Ever since his early years in Europe, Abel showed great interest in isolating pure form of internal gland hormones. The first work that led to his international reputation as a pharmacologist and biochemist was the isolation of epinephrine from adrenal medulla. However, he was only able to isolate a monobenzoyl derivative of epinephrine. While he was improving his processes on decomposing the benzoyl derivative to obtain salts of epinephrine using saponification, a Japanese chemist J. Takamine, who had visited his lab, was able

pos: Adrenal tumor anatomically at the center of each adrenal gland, and is composed of neuroendocrine (chromaffin) cells which produce and release epinephrine (adrenaline) into the bloodstream in response to activation of the sympathetic nervous system. Neuroblastoma and pheochromocytoma are the two most important tumors which arise from the adrenal medulla. Both tumors may also arise from extra-adrenal sites, specifically, in the paraganglia of the sympathetic chain. Neuroblastoma is an aggressive cancer of immature neuroblastic cells (precursors of neurons), and is one of the most common pediatric cancers, with a median age at diagnosis of two years. Adrenal neuroblastoma typically presents with a

pos: Smooth muscle and epinephrine (from sympathetic stimulation or the adrenal medulla) by producing vasoconstriction (this response is mediated through alpha-1 adrenergic receptors). However, blood vessels within skeletal muscle and cardiac muscle respond to these catecholamines producing vasodilation because the smooth muscle possess beta-adrenergic receptors. So there is a difference in the distribution of the various adrenergic receptors that explains the difference in why blood vessels from different areas respond to the same agent norepinephrine/epinephrine differently as well as differences due to varying amounts of these catecholamines that are released and sensitivities of various receptors to concentrations. Generally, arterial smooth muscle responds to

pos: Alpha-2 adrenergic receptor CNS structures: The α-adrenergic receptor is classically located on vascular prejunctional terminals where it inhibits the release of norepinephrine (noradrenaline) in a form of negative feedback. It is also located on the vascular smooth muscle cells of certain blood vessels, such as those found in skin arterioles or on veins, where it sits alongside the more plentiful α-adrenergic receptor. The α-adrenergic receptor binds both norepinephrine released by sympathetic postganglionic fibers and epinephrine (adrenaline) released by the adrenal medulla, binding norepinephrine with slightly higher affinity. It has several general functions in common with the α-adrenergic receptor, but also has specific effects

pos: Adrenal tumor localized disease, and chemotherapy for metastatic disease. Pheochromocytoma is a neoplasm composed of cells similar to the chromaffin cells of the mature adrenal medulla. Pheochromocytomas occur in patients of all ages, and may be sporadic, or associated with a hereditary cancer syndrome, such as multiple endocrine neoplasia (MEN) types IIA and IIB, neurofibromatosis type I, or von Hippel-Lindau syndrome. Only 10% of adrenal pheochromocytomas are malignant, while the rest are benign tumors. The most clinically important feature of pheochromocytomas is their tendency to produce large amounts of the catecholamine hormones epinephrine (adrenaline) and norepinephrine. This may lead to potentially life-threatening

pos: Repressed memory have for future avoidance behavior, and hormones that are released during stress have a role in determining what memories are preserved. In humans, traumatic stress is associated with acute secretion of epinephrine and norepinephrine (adrenaline and noradrenaline) from the adrenal medulla and cortisol from the adrenal cortex. Increases in these facilitate memory, but chronic stress associated with prolonged hypersecretion of cortisol may have the opposite effect. The limbic system is involved in memory storage and retrieval as well as giving emotional significance to sensory inputs. Within the limbic system, the hippocampus is important for explicit memory, and for memory consolidation;

pos: Muscarinic acetylcholine receptor form the principal receptors on the innervated tissue. Very few parts of the sympathetic system use cholinergic receptors. In sweat glands the receptors are of the "muscarinic" type. The sympathetic nervous system also has some preganglionic nerves terminating at the chromaffin cells in the adrenal medulla, which secrete epinephrine and norepinephrine into the bloodstream. Some believe that chromaffin cells are modified postganglionic CNS fibers. In the adrenal medulla, acetylcholine is used as a neurotransmitter, and the receptor is of the "nicotinic" type. The somatic nervous system uses a nicotinic receptor to acetylcholine at the neuromuscular junction. Muscarinic acetylcholine receptors are

pos: Nicotine are different by report: in particular it is both a stimulant and a relaxant. First causing a release of glucose from the liver and epinephrine (adrenaline) from the adrenal medulla, it causes stimulation. Users report feelings of relaxation, sharpness, calmness, and alertness. When a cigarette is smoked, nicotine-rich blood passes from the lungs to the brain within seven seconds and immediately stimulates nicotinic acetylcholine receptors; this indirectly promotes the release of many chemical messengers such as acetylcholine, norepinephrine, epinephrine, arginine vasopressin, serotonin, dopamine, and beta-endorphin in parts of the brain. Nicotine also increases the sensitivity of the brain's reward system

pos: Catecholamine such as norepinephrine have a hydroxyl group on the ethyl chain. Catecholamines are produced mainly by the chromaffin cells of the adrenal medulla and the postganglionic fibers of the sympathetic nervous system. Dopamine, which acts as a neurotransmitter in the central nervous system, is largely produced in neuronal cell bodies in two areas of the brainstem: the ventral tegmental area and the substantia nigra, the latter of which contains neuromelanin-pigmented neurons. The similarly neuromelanin-pigmented cell bodies of the locus ceruleus produce norepinephrine. Epinephrine is produced in small groups of neurons in the human brain which express its synthesizing enzyme, phenylethanolamine

pos: Autonomic dysreflexia its tonic firing, modulating its action on the peripheral sympathetic chain ganglia and the adrenal medulla. The sympathetic ganglia act directly on the blood vessels they innervate throughout the body, controlling vessel diameter and resistance, while the adrenal medulla indirectly controls the same action through the release of epinephrine and norepinephrine. The descending autonomic pathways, which are responsible for the supraspinal communication with the SPN, are interrupted resulting in decreased sympathetic outflow below the level of the injury. In this circumstance, the SPN is controlled only by spinal influences. The first couple weeks after a spinal injury, the decreased sympathetic

pos: Sympathoadrenal system to find. Diagnosis is also difficult because the symptoms are highly variable and very common in other diseases. If pheochromocytoma remains untreated, it may lead to fatal consequences especially to the cardiovascular system. Sympathoadrenal system The sympathoadrenal system is a physiological connection between the sympathetic nervous system and the adrenal medulla and is crucial in an organism’s physiological response to outside stimuli. When the body receives sensory information, the sympathetic nervous system sends a signal to preganglionic nerve fibers, which activate the adrenal medulla through acetylcholine. Once activated, norepinephrine and epinephrine are released directly into the blood by postganglionic nerve

pos: Sympathoadrenal system Sympathoadrenal system The sympathoadrenal system is a physiological connection between the sympathetic nervous system and the adrenal medulla and is crucial in an organism’s physiological response to outside stimuli. When the body receives sensory information, the sympathetic nervous system sends a signal to preganglionic nerve fibers, which activate the adrenal medulla through acetylcholine. Once activated, norepinephrine and epinephrine are released directly into the blood by postganglionic nerve fibers where they act as the bodily mechanism for "fight-or-flight" responses. Because of this, the sympathoadrenal system plays a large role in maintaining glucose levels, sodium levels, blood pressure, and various other metabolic

pos: Phenylethanolamine N-methyltransferase about one week to manifest a difference in PNMT levels. SAM not only acts as a cofactor for PNMT, but also helps to stabilize the enzyme and increase the half life by making it more resistant to being cut by trypsin protease. Epinephrine synthesis and therefore PNMT location has been largely found to be contained in the adrenal medulla or adrenal gland of most species. PNMT has been localized in most adult mammals to the cytoplasm of these medullary cells. Newer studies are also showing PNMT mRNA and protein to be expressed in other regions of the body as well.

pos: Heart rate is shortened. However, massive releases of these hormones coupled with sympathetic stimulation may actually lead to arrhythmias. There is no parasympathetic stimulation to the adrenal medulla. In general, increased levels of the thyroid hormones (thyroxine(T4) and triiodothyronine (T3)), increase the heart rate; excessive levels can trigger tachycardia. The impact of thyroid hormones is typically of a much longer duration than that of the catecholamines. The physiologically active form of triiodothyronine, has been shown to directly enter cardiomyocytes and alter activity at the level of the genome. It also impacts the beta adrenergic response similar to epinephrine and norepinephrine. Calcium ion

pos: Chromaffin cell nicotinic acetylcholine receptors on the adrenal medulla. This causes the release of catecholamines. The chromaffin cells release catecholamines: ~80% of adrenaline (epinephrine) and ~20% of noradrenaline (norepinephrine) into systemic circulation for systemic effects on multiple organs (similarly to secretory neurones of the hypothalamus), and can also send paracrine signals. Hence they are called neuroendocrine cells. There are two types of cells that originate from the neural crest and are related to the sympathetic nervous system (originate from a cell called sympathogonia): 1) Neuroblasts: These cells migrate, during the fourth to the fifth week of fetal development in humans, on both

pos: Sympathetic nervous system the great secretion of adrenaline (epinephrine) and to a lesser extent noradrenaline (norepinephrine) from it. Therefore, this response that acts primarily on the cardiovascular system is mediated directly via impulses transmitted through the sympathetic nervous system and indirectly via catecholamines secreted from the adrenal medulla. The sympathetic nervous system is responsible for priming the body for action, particularly in situations threatening survival. One example of this priming is in the moments before waking, in which sympathetic outflow spontaneously increases in preparation for action. Sympathetic nervous system stimulation causes vasoconstriction of most blood vessels, including many of those in the skin,

pos: Fight-or-flight response Fight-or-flight response The fight-or-flight response (also called hyperarousal, or the acute stress response) is a physiological reaction that occurs in response to a perceived harmful event, attack, or threat to survival. It was first described by Walter Bradford Cannon. His theory states that animals react to threats with a general discharge of the sympathetic nervous system, preparing the animal for fighting or fleeing. More specifically, the adrenal medulla produces a hormonal cascade that results in the secretion of catecholamines, especially norepinephrine and epinephrine. The hormones estrogen, testosterone, and cortisol, as well as the neurotransmitters dopamine and serotonin, also affect how

pos: Stressor after the stressor is transferred to the hypothalamus, which leads to the sympathetic nervous system. After which, the adrenal medulla secretes epinephrine. Mental and social stressors may affect behavior and how individuals respond to physical and chemical stressors. Life requires everyone to make sudden and planned adjustments to meet its demands, but the greater the demand comes with a greater adjustment and possibly more stress. Determining the impact of these various stressors allow individuals to decide the relationship between the types of stressors and the degree of distress. Identifying the stressor-stress relationship must involve quantifying the impact of life demands

pos: Adrenal gland disorder Adrenal gland disorder Adrenal gland disorders (or diseases) are conditions that interfere with the normal functioning of the adrenal glands. Adrenal disorders may cause hyperfunction or hypofunction, and may be congenital or acquired. The adrenal gland produces hormones that affects growth, development and stress, and also helps to regulate kidney function. There are two parts of the adrenal glands, the adrenal cortex and the adrenal medulla. The adrenal cortex produces mineralocorticoids, which regulate salt and water balance within the body, glucocorticoids (including cortisol) which have a wide number of roles within the body, and androgens, hormones with testosterone-like function. The

pos: Phenylethanolamine N-methyltransferase Phenylethanolamine N-methyltransferase Phenylethanolamine N-methyltransferase (PNMT) is an enzyme found primarily in the adrenal medulla that converts norepinephrine (noradrenaline) to epinephrine (adrenaline). It is also expressed in small groups of neurons in the human brain. PNMT is a protein whose encoding gene is found on chromosome 17 in humans. It consists of 4 exons and is a 30kDa protein. It shares many properties found among the other methyltransferases. It is closest in sequence to glycine-N-methyl transferase (GNMT). It also shares many structural properties like the shape of the folding lip with catechol-O-methyl transferase (COMT), though it shares less sequence identity. Several

pos: Phenylethanolamine N-methyltransferase replacement for the cofactor SAM, which resembles it, but is missing the methyl group, so no methyl transfer is possible. Phenylethanolamine N-methyltransferase Phenylethanolamine N-methyltransferase (PNMT) is an enzyme found primarily in the adrenal medulla that converts norepinephrine (noradrenaline) to epinephrine (adrenaline). It is also expressed in small groups of neurons in the human brain. PNMT is a protein whose encoding gene is found on chromosome 17 in humans. It consists of 4 exons and is a 30kDa protein. It shares many properties found among the other methyltransferases. It is closest in sequence to glycine-N-methyl transferase (GNMT). It also shares many

pos: Absent adrenal gland Absent adrenal gland Absent adrenal gland is a rare condition where the adrenal gland is absent at birth. It should not be confused with adrenal insufficiency or congenital adrenal hyperplasia, where the gland is present but may not be functioning adequately. Due to the absence of adrenal cortex, the condition causes extreme symptoms of adrenal insufficiency at birth due to very low levels of aldosterone and cortisol. The adrenal medulla can be normally present, poorly formed, or absent, however even so the effects of circulatory catecholamine deficiency are generally mild (due to sympathetic nervous system compensation), except in episodes of

pos: Chromaffin cell the liver. In non-mammals, chromaffin cells are found in a variety of places, generally not organised as an individual organ, and may be without innervation, relying only on endocrine or paracrine signals for secretion. Chromaffin cells of the adrenal medulla are innervated by the splanchnic nerve and secrete adrenaline (epinephrine), noradrenaline (norepinephrine), some dopamine, enkephalin and enkephalin-containing peptides, and a few other hormones into the blood stream. The secreted adrenaline and noradrenaline play an important role in the sympathetic nervous system response, commonly called the fight-or-flight response. The enkephalins and enkephalin-containing peptides are related to, but distinct from endogenous peptides

pos: Tyrosine hydroxylase Tyrosine hydroxylase Tyrosine hydroxylase or tyrosine 3-monooxygenase is the enzyme responsible for catalyzing the conversion of the amino acid -tyrosine to -3,4-dihydroxyphenylalanine (-DOPA). It does so using molecular oxygen (O), as well as iron (Fe) and tetrahydrobiopterin as cofactors. -DOPA is a precursor for dopamine, which, in turn, is a precursor for the important neurotransmitters norepinephrine (noradrenaline) and epinephrine (adrenaline). Tyrosine hydroxylase catalyzes the rate limiting step in this synthesis of catecholamines. In humans, tyrosine hydroxylase is encoded by the "TH" gene, and the enzyme is present in the central nervous system (CNS), peripheral sympathetic neurons and the adrenal medulla.

pos: Vesicular monoamine transporter medulla cells whereas VMAT2 is the major transporter in the bovine adrenal medulla cells. Both isoforms of VMAT, VMAT1 and VMAT2, are acidic glycoproteins with a molecular weight of approximately 70 kDa. Both isoforms are transmembrane proteins with 12 transmembrane domains (TMD’s). VMAT functions in loading the neurotransmitters dopamine, serotonin, histamine, norepinephrine, and epinephrine into transport vesicles. Collectively these neurotransmitters are referred to as monoamines. VMAT uses the same transport mechanism for all types of monoamines. VMATs transport monoamines from the cytosol into high-concentration storage vesicles. Transport vesicles are released into the space between neurons, called the synaptic cleft, where

pos: Norepinephrine can either be broken down by monoamine oxidase or repackaged into vesicles by VMAT, making it available for future release. Norepinephrine is the main neurotransmitter used by the sympathetic nervous system, which consists of about two dozen sympathetic chain ganglia located next to the spinal cord, plus a set of prevertebral ganglia located in the chest and abdomen. These sympathetic ganglia are connected to numerous organs, including the eyes, salivary glands, heart, lungs, liver, gallbladder, stomach, intestines, kidneys, urinary bladder, reproductive organs, muscles, skin, and adrenal glands. Sympathetic activation of the adrenal glands causes the part called the adrenal medulla

pos: Vesicular monoamine transporter 1 cells, in contrast to VMAT2, which is also found in the PNS and CNS. Specifically, VMAT1 is found in chromaffin cells, enterochromaffin cells, and small intensely fluorescent cells (SIFs). Chromaffin cells are responsible for releasing the catecholamines (norepinephrine and epinephrine) into systemic circulation. Enterochromaffin cells are responsible for storing serotonin in the gastrointestinal tract. SIFs are interneurons associated with the sympathetic nervous system which are managed by dopamine. VMAT1 is found in both large dense-core vesicles (LDCVs) as well as in small synaptic vesicles (SSVs). This was discovered via studying rat adrenal medulla cells (PC12 cells). LDCVs are 70-200 nm

pos: Adrenal gland small arteries may enter each gland. Three arteries usually supply each adrenal gland: These blood vessels supply a network of small arteries within the capsule of the adrenal glands. Thin strands of the capsule enter the glands, carrying blood to them. Venous blood is drained from the glands by the suprarenal veins, usually one for each gland: The central adrenomedullary vein, in the adrenal medulla, is an unusual type of blood vessel. Its structure is different from the other veins in that the smooth muscle in its tunica media (the middle layer of the vessel) is arranged in conspicuous, longitudinally

pos: Adrenal gland steroid hormone synthesis and expressed in cortical cell layers, and PNMT and DBH involved in noradrenalin and adrenalin synthesis and expressed in the medulla. The adrenal glands are composed of two heterogenous types of tissue. In the center is the adrenal medulla, which produces adrenaline and noradrenaline and releases them into the bloodstream, as part of the sympathetic nervous system. Surrounding the medulla is the cortex, which produces a variety of steroid hormones. These tissues come from different embryological precursors and have distinct prenatal development paths. The cortex of the adrenal gland is derived from mesoderm, whereas the medulla is

neg: Pheochromocytoma Pheochromocytoma Pheochromocytoma (PCC) is a neuroendocrine tumor of the medulla of the adrenal glands (originating in the chromaffin cells), or extra-adrenal chromaffin tissue that failed to involute after birth, that secretes high amounts of catecholamines, mostly norepinephrine, plus epinephrine to a lesser extent. Extra-adrenal paragangliomas (often described as extra-adrenal pheochromocytomas) are closely related, though less common, tumors that originate in the ganglia of the sympathetic nervous system and are named based upon the primary anatomical site of origin. The term is from the Greek "phaios" (dark), "chroma" (color), "kytos" (cell), and "-oma" (tumor). The signs and symptoms of a pheochromocytoma

neg: Pheochromocytoma 1970s, Greene and Tischler derived a line of cells, called the PC12 cell line, from a rat pheochromocytoma. Pheochromocytoma Pheochromocytoma (PCC) is a neuroendocrine tumor of the medulla of the adrenal glands (originating in the chromaffin cells), or extra-adrenal chromaffin tissue that failed to involute after birth, that secretes high amounts of catecholamines, mostly norepinephrine, plus epinephrine to a lesser extent. Extra-adrenal paragangliomas (often described as extra-adrenal pheochromocytomas) are closely related, though less common, tumors that originate in the ganglia of the sympathetic nervous system and are named based upon the primary anatomical site of origin. The term is from

neg: Horse behavior a prey species. The fight-or-flight response involves nervous impulses which result in hormone secretions into the bloodstream. When a horse reacts to a threat, it may initially "freeze" in preparation to take flight. The fight-or-flight reaction begins in the brain amygdala, which triggers a neural response in the hypothalamus. The initial reaction is followed by activation of the pituitary gland and secretion of the hormone ACTH. The adrenal gland is activated almost simultaneously and releases the neurotransmitters epinephrine (adrenaline) and norepinephrine (noradrenaline). The release of chemical messengers results in the production of the hormone cortisol, which increases blood pressure and

neg: Cortisol mainly secreting the catecholamines adrenaline (epinephrine) and noradrenaline (norepinephrine) under sympathetic stimulation. The synthesis of cortisol in the adrenal gland is stimulated by the anterior lobe of the pituitary gland with ACTH; ACTH production is, in turn, stimulated by CRH, which is released by the hypothalamus. ACTH increases the concentration of cholesterol in the inner mitochondrial membrane, via regulation of the steroidogenic acute regulatory protein. It also stimulates the main rate-limiting step in cortisol synthesis, in which cholesterol is converted to pregnenolone and catalyzed by cytochrome P450SCC (side-chain cleavage enzyme). Cortisol is metabolized by the 11-beta hydroxysteroid dehydrogenase system (11-beta

neg: Traumatic memories compared to the ease with which they fire without the drug present. Using U0 126, researchers were able to selectively knock out a fear memory for a specific audio tone and leave a fear memory for another audio tone in a group of rats. This was observed by recording brain activity in the amygdala of these rats when presented with tones they had been conditioned to fear. Propranolol is a blocker for the beta-adrenergic receptors in the amygdala which usually are bound to by stress hormones released by the adrenal gland- epinephrine and norepinephrine. Research exploring the idea that blocking

neg: Adrenal gland the presence of certain molecules of the inflammatory response. Mineralocorticoid secretion is regulated mainly by the renin–angiotensin–aldosterone system (RAAS), the concentration of potassium, and to a lesser extent the concentration of ACTH. Sensors of blood pressure in the juxtaglomerular apparatus of the kidneys release the enzyme renin into the blood, which starts a cascade of reactions that lead to formation of angiotensin II. Angiotensin receptors in cells of the zona glomerulosa recognize the substance, and upon binding they stimulate the release of aldosterone. Primarily referred to in the United States as epinephrine and norepinephrine, adrenaline and noradrenaline are catecholamines, water-soluble

neg: Adrenaline below the detection limit in the blood stream. The adrenal glands contribute about 7% of circulating norepinephrine, most of which is a spill over from neurotransmission with little activity as a hormone. Pharmacological doses of epinephrine stimulate α, α, β, β, and β adrenoceptors of the sympathetic nervous system. Sympathetic nerve receptors are classified as adrenergic, based on their responsiveness to adrenaline. The term "adrenergic" is often misinterpreted in that the main sympathetic neurotransmitter is norepinephrine (noradrenaline), rather than epinephrine, as discovered by Ulf von Euler in 1946. Epinephrine does have a β adrenoceptor-mediated effect on metabolism and the airway,

neg: Cell signaling called hormones. Hormones are produced by endocrine cells and they travel through the blood to reach all parts of the body. Specificity of signaling can be controlled if only some cells can respond to a particular hormone. "Paracrine" signals such as retinoic acid target only cells in the vicinity of the emitting cell. Neurotransmitters represent another example of a paracrine signal. Some signaling molecules can function as both a hormone and a neurotransmitter. For example, epinephrine and norepinephrine can function as hormones when released from the adrenal gland and are transported to the heart by way of the blood stream.

neg: Arteriole to an increase in flow rate. Arterioles receive autonomic nervous system innervation and respond to various circulating hormones in order to regulate their diameter. Retinal vessels lack a functional sympathetic innervation. Further local responses to stretch, carbon dioxide, pH, and oxygen also influence arteriolar tone. Generally, norepinephrine and epinephrine (hormones produced by sympathetic nerves and the adrenal gland medulla) are vasoconstrictive acting on alpha 1-adrenergic receptors. However, the arterioles of skeletal muscle, cardiac muscle, and pulmonary circulation vasodilate in response to these hormones when they act on beta-adrenergic receptors. Generally, stretch and high oxygen tension increase tone, and carbon dioxide

neg: Thomas C. Südhof the structure and function of chromaffin cells which are responsible for the release of epinephrine, norepinephrine and endorphins from the medulla of the adrenal gland. Innervated by sympathetic nervous system, chromaffin cells are important in the initiation of the fight-or-flight response of animals when exposed to threatening stimuli. After completing his thesis in 1983, Südhof moved to UT Southwestern Medical Center for his postdoctoral training where he began researching in the department of molecular genetics under the supervision of Joseph L. Goldstein and Michael Stuart Brown. While a postdoctoral fellow, Südhof cloned the gene for the low-density lipoprotein receptor and,

neg: Adrenal gland oriented bundles. The adrenal glands may not develop at all, or may be fused in the midline behind the aorta. These are associated with other congenital abnormalities, such as failure of the kidneys to develop, or fused kidneys. The gland may develop with a partial or complete absence of the cortex, or may develop in an unusual location. The adrenal gland secretes a number of different hormones which are metabolised by enzymes either within the gland or in other parts of the body. These hormones are involved in a number of essential biological functions. Corticosteroids are a group of steroid

neg: Head and neck anatomy through the circulatory system and by direct connection of neurons. Also, within the cranium, the pineal gland, which attaches to the thalamus, controls the body's 24-hour rhythms circadian rhythm through the release of melatonin. The pituitary gland secretes hormones that directly impact the body as well as hormones that indirectly control body functions because they activate other endocrine glands, such as the adrenal cortex (ACTH) and the thyroid gland (TSH). These two glands when stimulated by pituitary hormones then release their own hormones. The pituitary gland has two lobes, the anterior lobe and the posterior lobe. The anterior lobe secretes:

neg: Acute stress reaction colloquially known as the "fight or flight" response, indicated by accelerated pulse and respiration rates, pupil dilation, and a general feeling of anxiety and hyper-awareness. This is caused by the release of epinephrine and norepinephrine from the adrenal glands. The epinephrine and norepinephrine strike the beta receptors of the heart, which feeds the heart sympathetic nerve fibers in order to increase the strength of heart muscle contraction; as a result more blood gets circulated, increasing the heart rate and respiratory rate. The sympathetic nervous system also stimulates the skeletal system and muscular system in an effort to pump more blood

neg: Negative feedback resulting in diabetes. For hormone secretion regulated by the negative feedback loop: when gland X releases hormone X, this stimulates target cells to release hormone Y. When there is an excess of hormone Y, gland X "senses" this and inhibits its release of hormone X. As shown in the figure, most endocrine hormones are controlled by a physiologic negative feedback inhibition loop, such as the glucocorticoids secreted by the adrenal cortex. The hypothalamus secretes corticotropin-releasing hormone (CRH), which directs the anterior pituitary gland to secrete adrenocorticotropic hormone (ACTH). In turn, ACTH directs the adrenal cortex to secrete glucocorticoids, such as

neg: Norepinephrine types of cancer. The consequence is a massive increase in the amount of norepinephrine and epinephrine released into the bloodstream. The most obvious symptoms are those of sympathetic hyperactivation, including particularly a rise in blood pressure that can reach fatal levels. The most effective treatment is surgical removal of the tumor. Stress, to a physiologist, means any situation that threatens the continued stability of the body and its functions. Stress affects a wide variety of body systems: the two most consistently activated are the hypothalamic-pituitary-adrenal axis and the norepinephrine system, including both the sympathetic nervous system and the locus coeruleus-centered

neg: Stress in early childhood but impacts the brain for a longer period of time. In conjunction, the SAM and HPA systems work to regulate stress and unite at the hypothalamus, which in turn regulates behavior. In humans, there are chromaffin cells in the adrenal glands (medulla) that get stimulated through the sympathetic nervous system during a stress response. These cells release the hormones epinephrine and norepinephrine (NE). Epinephrine and NE bind to receptors of target organs and instigate the fight or flight response. As an example, epinephrine increases heart rate and causes blood vessels to dilate in muscles and blood vessels to constrict in

neg: Adrenal gland blood pressure, and constriction of blood vessels in many parts of the body. Catecholamines are produced in chromaffin cells in the medulla of the adrenal gland, from tyrosine, a non-essential amino acid derived from food or produced from phenylalanine in the liver. The enzyme tyrosine hydroxylase converts tyrosine to L-DOPA in the first step of catecholamine synthesis. L-DOPA is then converted to dopamine before it can be turned into noradrenaline. In the cytosol, noradrenaline is converted to epinephrine by the enzyme phenylethanolamine N-methyltransferase (PNMT) and stored in granules. Glucocorticoids produced in the adrenal cortex stimulate the synthesis of catecholamines by

neg: Vanillylmandelic acid per 24 hours) is assessed along with creatinine clearance, and the quantity of cortisols, catecholamines, and metanephrines excreted is also measured. Urinary VMA is elevated in patients with tumors that secrete catecholamines. These urinalysis tests are used to diagnose an adrenal gland tumor called pheochromocytoma, a tumor of catecholamine-secreting chromaffin cells. These tests may also be used to diagnose neuroblastomas, and to monitor treatment of these conditions. Norepinephrine is metabolised into normetanephrine and VMA. Norepinephrine is one of the hormones produced by the adrenal glands, which are found on top of the kidneys. These hormones are released into the blood

neg: Adrenal gland protein and the stimulation of synthesis of glucose from these amino acids in the liver. In addition, they increase the levels of free fatty acids, which cells can use as an alternative to glucose to obtain energy. Glucocorticoids also have effects unrelated to the regulation of blood sugar levels, including the suppression of the immune system and a potent anti-inflammatory effect. Cortisol reduces the capacity of osteoblasts to produce new bone tissue and decreases the absorption of calcium in the gastrointestinal tract. The adrenal gland secretes a basal level of cortisol but can also produce bursts of the hormone in

neg: Adrenocortical hormone an adrenal tumor or by hypersecretion of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland. It is predominantly due to an excess of the glucocorticoid cortisol. Secretion is typically regulated by the hypothalamus which secretes corticotropin-releasing hormone (CRH) to the pituitary gland, stimulating the pituitary to secrete adrenocorticotropic hormone (ACTH). ACTH then travels to the adrenal glands and induces the release of cortisol into the bloodstream. In Cushing’s syndrome, this process occurs in excess. Some symptoms of an individual with Cushing’s syndrome include low tissue protein levels, due to muscle and bone atrophy, and high blood glucose levels. Sodium levels

neg: Cardiac physiology the force of contractions. Sympathetic stimulation triggers the release of norepinephrine from the cardiac nerves and also stimulates the adrenal cortex to secrete both epinephrine and norepinephrine. These secretions increase the heart rate, subsequent metabolic rate and contractility. Parasympathetic stimulation stimulates the release of acetylcholine (ACh) from the vagus nerve which decreases contractility, and stroke volume which increases end systolic volume. Several synthetic drugs have been developed that can act either as a stimulant or inhibitor inotrope. The stimulant inotropes, such as Digoxin, cause higher concentrations of calcium ions which increase contractility. Excess calcium (hypercalcemia) is also a positive inotrope.

neg: Fight-or-flight response is followed by activation of the pituitary gland and secretion of the hormone ACTH. The adrenal gland is activated almost simultaneously, via the sympathetic nervous system, and releases the hormone epinephrine. The release of chemical messengers results in the production of the hormone cortisol, which increases blood pressure, blood sugar, and suppresses the immune system. The initial response and subsequent reactions are triggered in an effort to create a boost of energy. This boost of energy is activated by epinephrine binding to liver cells and the subsequent production of glucose. Additionally, the circulation of cortisol functions to turn fatty acids

neg: Sympathoadrenal system a single unit to activate an organism’s “fight or flight” response. This “sympathoadrenal discharge” causes an increase in heart rate, cardiac output, blood pressure, and glucose levels. These sympathoadrenal functions show the combined responses of the central nervous system on a multitude of external stimuli. The two main chemical messengers of the sympathoadrenal system are norepinephrine and epinephrine (also called noradrenaline and adrenaline respectively). These chemicals are created by the adrenal glands after receiving neuronal signals from the sympathetic nervous system. The different physiological affects of these chemicals depend on the particular tissue that it innervates. As part of the

neg: Epinephrine (medication) pressure, it lowers carotid blood flow and end-tidal CO or ECO levels. It appears that epinephrine may be improving macrocirculation at the expense of the capillary beds where actual perfusion is taking place. Extracts of the adrenal gland were first obtained by Polish physiologist Napoleon Cybulski in 1895. These extracts, which he called "nadnerczyna", contained adrenaline and other catecholamines. American ophthalmologist William H. Bates discovered adrenaline's usage for eye surgeries prior to 20 April 1896. Japanese chemist Jokichi Takamine and his assistant Keizo Uenaka independently discovered adrenaline in 1900. In 1901, Takamine successfully isolated and purified the hormone from the

neg: Marriage and health produced by the sympathetic-adrenal-medullary axis (SAM) and hypothalamic-pituitary-adrenal axis (HPA) have wide-ranging effects across the body. Both axes have been implicated in the links between psychological factors and physical health. SAM activity can be measured by levels of circulating catecholamines—epinephrine and norepinephrine. Negative interactions with one's spouse have been linked to elevated catecholamine levels, both during and after conflict. Daily fluctuations in the level of cortisol—a stress hormone—are an important marker of health; flatter slopes of cortisol change throughout the day are strongly associated with cardiovascular disease and related mortality. Lower marital satisfaction has been linked with flatter cortisol slopes

neg: Stress in early childhood or frequent biological stress response may increase the risk for future physical and mental health problems in early childhood. Since, brain circuits are vulnerable in early childhood, early stressors may impact the development of necessary brain connections. Therefore, toxic stress can alter or impair brain circuit formation and essentially result in a small brain size in young children. In humans, the stress response pathway consists of the sympathetic-adrenomedullary (SAM) system and the hypothalamic-pituitary-adrenal axis (HPA). The SAM system is a part of the sympathetic component of the autonomic nervous system. These systems are responsible for releasing epinephrine and norepinephrine (NE),

neg: Conditioned place preference that has been extinguished over two weeks. When rats experience stress in the form of foot-shock or noise, changes occur in the norepinephrine system and the hypothalamic-pituitary-adrenal axis. These changes have a high impact on the reinstatement conditioned place preference. Stress stimulates the release of corticotropin-releasing hormone (CRH) from the rat's hypothalamus which leads to a series of changes through the pituitary gland in the brain to release glucocorticoids from the adrenal glands. CRH also stimulates the release of neurotransmitter in the hypothalamic regions of the brain to mediate stress-induced changes in brain activity This system plays a key role

neg: Norepinephrine reuptake inhibitor transporters (MATs) are listed here. For a list of NRIs that act at multiple MATs, see the other monoamine reuptake inhibitor pages such as NDRI, SNRI, and SNDRI. Norepinephrine reuptake inhibitor A norepinephrine reuptake inhibitor (NRI, NERI) or adrenergic reuptake inhibitor (ARI), is a type of drug that acts as a reuptake inhibitor for the neurotransmitters norepinephrine (noradrenaline) and epinephrine (adrenaline) by blocking the action of the norepinephrine transporter (NET). This in turn leads to increased extracellular concentrations of norepinephrine and epinephrine and therefore can increase in adrenergic neurotransmission. NRIs are commonly used in the treatment of conditions like ADHD

neg: Endurance running hypothesis advantage of being able to alter their diet to meet these prolonged energy demands. In addition to flexibility in the utilization of energy, hominins have evolved larger thyroid and adrenal glands which enable them to utilize the energy in carbohydrates and fatty acids more readily and efficiently. These organs are responsible for releasing hormones including epinephrine, norepinephrine, adrenocorticotropic hormone (ACTH), glucagon, and thyroxine. Larger glands allows for greater production of these key hormones and ultimately, maximized utilization of stored fuel. Taken together, the flexibility in diet and the enhanced usage of fuel heightens the previously mentioned finding that, unlike quadrupeds,

neg: Anger to the neocortex. Based on some statistical analysis, some scholars have suggested that the tendency for anger may be genetic. Distinguishing between genetic and environmental factors however requires further research and actual measurement of specific genes and environments. The external expression of anger can be found in physiological responses, facial expressions, body language, and at times in public acts of aggression. The rib cage tenses and breathing through the nose becomes faster, deeper, and irregular. Anger activates the hypothalamic–pituitary–adrenal axis. The catecholamine activation is more strongly norepinephrine than epinephrine. Heart rate and blood pressure increase. Blood flows to the hands.

neg: Peptide hormone released into the blood. When a peptide hormone binds to a receptor on the surface of the cell, a second messenger appears in the cytoplasm, which triggers signal transduction leading to the cellular responses. Some peptide/protein hormones (angiotensin II, basic fibroblast growth factor-2, parathyroid hormone-related protein) also interact with intracellular receptors located in the cytoplasm or nucleus by an intracrine mechanism. Several important peptide hormones are secreted from the pituitary gland. The anterior pituitary secretes three hormones: prolactin, which acts on the mammary gland; adrenocorticotropic hormone (ACTH), which acts on the adrenal cortex to regulate the secretion of glucocorticoids; and

neg: Norepinephrine reuptake inhibitor Norepinephrine reuptake inhibitor A norepinephrine reuptake inhibitor (NRI, NERI) or adrenergic reuptake inhibitor (ARI), is a type of drug that acts as a reuptake inhibitor for the neurotransmitters norepinephrine (noradrenaline) and epinephrine (adrenaline) by blocking the action of the norepinephrine transporter (NET). This in turn leads to increased extracellular concentrations of norepinephrine and epinephrine and therefore can increase in adrenergic neurotransmission. NRIs are commonly used in the treatment of conditions like ADHD and narcolepsy due to their psychostimulant effects and in obesity due to their appetite suppressant effects. They are also frequently used as antidepressants for the treatment of major

neg: Social defeat also implicates that the referred behavioral effects are moderated by neuroendocrine phenomena involving serotonin, dopamine, epinephrine, norepinephrine, and in the hypothalamic-pituitary-adrenal axis, locus ceruleus and limbic systems (Bjorkqvist, 2001; Rygula et alli, 2005; Selten & Cantor-Graae, 2005; Marinia et alli, 2006; Huhman, 2006). Both animal and human studies suggest that the social environment has a strong influence on the consequences of stresses. This finding seems to be especially true in the case of social stresses, like social defeat (Bjorkqvist, 2001; Rygula et alli, 2005; de Jong et alli, 2005). In animal studies, animals housed collectively showed reduced symptoms after defeat,

neg: Norepinephrine releasing agent also a nicotinic acetylcholine receptor antagonist. Norepinephrine releasing agent A norepinephrine releasing agent (NRA), also known as an adrenergic releasing agent, is a catecholaminergic type of drug which induces the release of norepinephrine (noradrenaline) and epinephrine (adrenaline) from the pre-synaptic neuron into the synapse. This in turn leads to increased extracellular concentrations of norepinephrine and epinephrine therefore an increase in adrenergic neurotransmission. A closely related type of drug is a norepinephrine reuptake inhibitor (NRI). Another class of drugs that stimulates adrenergic activity is the adrenergic receptor agonist class. NRAs are used for a variety of clinical indications including the following:

neg: Norepinephrine releasing agent Norepinephrine releasing agent A norepinephrine releasing agent (NRA), also known as an adrenergic releasing agent, is a catecholaminergic type of drug which induces the release of norepinephrine (noradrenaline) and epinephrine (adrenaline) from the pre-synaptic neuron into the synapse. This in turn leads to increased extracellular concentrations of norepinephrine and epinephrine therefore an increase in adrenergic neurotransmission. A closely related type of drug is a norepinephrine reuptake inhibitor (NRI). Another class of drugs that stimulates adrenergic activity is the adrenergic receptor agonist class. NRAs are used for a variety of clinical indications including the following: They are also used as recreational

neg: Absent adrenal gland hypoglycemia. SF-1 plays a role in the development of adrenal gland. Single gene polymorphism involving SF-1 gene may have a role in adrenal gland agenesis. Various other factors have also been identified. Absent adrenal gland Absent adrenal gland is a rare condition where the adrenal gland is absent at birth. It should not be confused with adrenal insufficiency or congenital adrenal hyperplasia, where the gland is present but may not be functioning adequately. Due to the absence of adrenal cortex, the condition causes extreme symptoms of adrenal insufficiency at birth due to very low levels of aldosterone and cortisol. The

neg: Phenylethanolamine N-methyltransferase and deactivation pathways. PNMT is also involved in the biosynthesis of "N"-methylated trace amines: it metabolizes phenethylamine into "N"-methylphenethylamine (a positional isomer of amphetamine), "p"-octopamine into synephrine, and "p"-tyramine into "N"-methyltyramine. Elevated PNMT expression is one of the ways that the stress response positively feeds back on itself. An increase in stress hormones or nerve impulses due to stress can cause PNMT to convert more norepinephrine into epinephrine. This increases the potency of the catecholamine response system, increasing the sympathetic output and making the stress response more profound. PNMT is known to be regulated by glucocorticoids made in the adrenal

neg: Vasodilation (e.g., nitric oxide, bradykinin, potassium ions, and adenosine), as well as an organism's autonomic nervous system and adrenal glands, both of which secrete catecholamines such as norepinephrine and epinephrine, respectively. Vasodilation is the result of relaxation in smooth muscle surrounding the blood vessels. This relaxation, in turn, relies on removing the stimulus for contraction, which depends on intracellular calcium ion concentrations and is tightly linked with phosphorylation of the light chain of the contractile protein myosin. Thus, vasodilation works mainly either by lowering intracellular calcium concentration or by dephosphorylation (really substitution of ATP for ADP) of myosin. Dephosphorylation by myosin

neg: Julius Axelrod Julius Axelrod Julius Axelrod (May 30, 1912 – December 29, 2004) was an American biochemist. He won a share of the Nobel Prize in Physiology or Medicine in 1970 along with Bernard Katz and Ulf von Euler. The Nobel Committee honored him for his work on the release and reuptake of catecholamine neurotransmitters, a class of chemicals in the brain that include epinephrine, norepinephrine, and, as was later discovered, dopamine. Axelrod also made major contributions to the understanding of the pineal gland and how it is regulated during the sleep-wake cycle. Axelrod was born in New York City, the son

neg: Circumventricular organs that directly extend from cell bodies in the hypothalamus, through the infundibulum. It is located in the sella turcica of the sphenoid bone at the base of the skull. The pituitary is sometimes referred to as the “master gland” because it has a crucial role in maintaining homeostasis and guiding the activity of other glands. The anterior lobe secretes growth hormone, prolactin and tropic hormones for the thyroid, gonads and adrenal glands. The posterior lobe stores and releases oxytocin and vasopressin, also known as antidiuretic hormone (ADH), which are produced in the hypothalamus. The median eminence (ME) is located in

neg: Stressor stressors may produce pain and impair work performance. Chronic pain and impairment requiring medical attention may result from extreme physical stressors or if there is not sufficient recovery time between successive exposures. Stressors may also affect mental function and performance. One possible mechanism involves stimulation of the hypothalamus, CRF (corticotropin release factor) -> pituitary gland releases ACTH (adrenocorticotropic hormone) -> adrenal cortex secretes various stress hormones (e.g., cortisol) -> stress hormones (30 varieties) travel in the blood stream to relevant organs, e.g., glands, heart, intestines -> flight-or-fight response. Between this flow there is an alternate path that can be taken

neg: Sympathetic nervous system the digestive tract, and the kidneys. This occurs as a result of activation of alpha-1 adrenergic receptors by norepinephrine released by post-ganglionic sympathetic neurons. These receptors exist throughout the vasculature of the body but are inhibited and counterbalanced by beta-2 adrenergic receptors (stimulated by epinephrine release from the adrenal glands) in the skeletal muscles, the heart, the lungs, and the brain during a sympathoadrenal response. The net effect of this is a shunting of blood away from the organs not necessary to the immediate survival of the organism and an increase in blood flow to those organs involved in intense

neg: Insulin conflicting influences on insulin release by beta cells, because insulin release is inhibited by α-adrenergic receptors and stimulated by β-adrenergic receptors. The net effect of norepinephrine from sympathetic nerves and epinephrine from adrenal glands on insulin release is inhibition due to dominance of the α-adrenergic receptors. When the glucose level comes down to the usual physiologic value, insulin release from the β-cells slows or stops. If the blood glucose level drops lower than this, especially to dangerously low levels, release of hyperglycemic hormones (most prominently glucagon from islet of Langerhans alpha cells) forces release of glucose into the blood from

neg: Adrenal insufficiency disease, and autoimmune gastritis with pernicious anemia. Adrenoleukodystrophy can also cause adrenal insufficiency. Adrenal insufficiency can also result when a patient has a craniopharyngioma, which is a histologically benign tumor that can damage the pituitary gland and so cause the adrenal glands not to function. This would be an example of secondary adrenal insufficiency syndrome. Causes of adrenal insufficiency can be categorized by the mechanism through which they cause the adrenal glands to produce insufficient cortisol. These are adrenal dysgenesis (the gland has not formed adequately during development), impaired steroidogenesis (the gland is present but is biochemically unable to produce

neg: Adrenal gland Reichstein were then awarded the 1950 Nobel Prize in Physiology or Medicine for their discoveries on the structure and effects of the adrenal hormones. Adrenal gland The adrenal glands (also known as suprarenal glands) are endocrine glands that produce a variety of hormones including adrenaline and the steroids aldosterone and cortisol. They are found above the kidneys. Each gland has an outer cortex which produces steroid hormones and an inner medulla. The adrenal cortex itself is divided into three zones: the zona glomerulosa, the zona fasciculata and the zona reticularis. The adrenal cortex produces three main types of steroid hormones:

neg: Adrenal gland disease and genetic causes) directly affect the adrenal cortex. If a problem that affects the hypothalamic-pituitary-adrenal axis arises outside the gland, it is a "secondary adrenal insufficiency". Addison's disease refers to primary hypoadrenalism, which is a deficiency in glucocorticoid and mineralocorticoid production by the adrenal gland. In the Western world, Addison's disease is most commonly an autoimmune condition, in which the body produces antibodies against cells of the adrenal cortex. Worldwide, the disease is more frequently caused by infection, especially from tuberculosis. A distinctive feature of Addison's disease is hyperpigmentation of the skin, which presents with other nonspecific symptoms such

neg: Hyperandrogenism endogenous, depending on whether it is caused by an external or internal source, respectively. The intake of glucocorticoids, which are a type of steroid hormone, is a common cause for the development of exogenous Cushing's syndrome. Endogenous Cushing's syndrome can occur when the body produces excessive amounts of cortisol. This occurs when the hypothalamus of the brain transmits corticotropin-releasing hormone (CRH) to the pituitary gland, which in turn secretes adrenocorticotropin hormone (ACTH). ACTH then causes the adrenal glands to release cortisol into the blood. Signs of Cushing's syndrome include muscle weakness, easy bruising, weight gain, male-pattern hair growth (hirsutism), colored

neg: Adrenal gland by the placenta for estrogen biosynthesis. Cortical development of the adrenal gland is regulated mostly by ACTH, a hormone produced by the pituitary gland that stimulates cortisol synthesis. During midgestation, the fetal zone occupies most of the cortical volume and produces 100–200 mg/day of DHEA-S, an androgen and precursor of both androgens and estrogens (female sex hormones). Adrenal hormones, especially glucocorticoids such as cortisol, are essential for prenatal development of organs, particularly for the maturation of the lungs. The adrenal gland decreases in size after birth because of the rapid disappearance of the fetal zone, with a corresponding decrease in

neg: Adrenal gland Adrenal gland The adrenal glands (also known as suprarenal glands) are endocrine glands that produce a variety of hormones including adrenaline and the steroids aldosterone and cortisol. They are found above the kidneys. Each gland has an outer cortex which produces steroid hormones and an inner medulla. The adrenal cortex itself is divided into three zones: the zona glomerulosa, the zona fasciculata and the zona reticularis. The adrenal cortex produces three main types of steroid hormones: mineralocorticoids, glucocorticoids, and androgens. Mineralocorticoids (such as aldosterone) produced in the zona glomerulosa help in the regulation of blood pressure and electrolyte balance. The

neg: Rage (emotion) when oxytocin, vasopressin, and corticotropin-releasing hormone are rapidly released from the hypothalamus. This results in the pituitary gland producing and releasing large amounts of the adrenocorticotropic hormone, which causes the adrenal cortex to release corticosteroids. This chain reaction occurs when faced with a threatening situation. Nearly two decades later, more came to be known about the impacts of high epinephrine. As the focus in neuroscience began to shift towards the roles of white matter tissues, a more full bodied understanding of this complex emotion was able to be extrapolated. Memory, being the “retention of perceptions”, can be viewed as a

neg: History of catecholamine research "Nobel Prize in Physiology or Medicine" ″for their discoveries of important principles for drug treatment″, Black's ″important principles″ being the blockade of β-adrenoceptors and of histamine H receptors. In 2012, Robert Lefkowitz and Brian Kobilka shared the Nobel Prize in Chemistry ″for studies of G-protein-coupled receptors″. History of catecholamine research The catecholamines comprise the endogenous substances dopamine, noradrenaline (norepinephrine) and adrenaline (epinephrine) as well as numerous artificially synthesized compounds such as isoprenaline. Their investigation constitutes a prominent chapter in the history of physiology, biochemistry and pharmacology. Adrenaline was the first hormone extracted from its endocrine gland and obtained in pure

neg: History of catecholamine research History of catecholamine research The catecholamines comprise the endogenous substances dopamine, noradrenaline (norepinephrine) and adrenaline (epinephrine) as well as numerous artificially synthesized compounds such as isoprenaline. Their investigation constitutes a prominent chapter in the history of physiology, biochemistry and pharmacology. Adrenaline was the first hormone extracted from its endocrine gland and obtained in pure form, before the word "hormone" was coined. It was also the first hormone the structure and biosynthesis of which were clarified. Apart from acetylcholine, adrenaline and noradrenaline were the first neurotransmitters to be discovered and the first intercellular biochemical signals to be found in intracellular vesicles.

neg: Adrenal gland a characteristic not present in all sympathetic organs. Glucocorticoids produced in the adrenal cortex were once thought to be responsible for the differentiation of chromaffin cells. More recent research suggests that BMP-4 secreted in adrenal tissue is the main responsible for this, and that glucocorticoids only play a role in the subsequent development of the cells. The normal function of the adrenal gland may be impaired by conditions such as infections, tumors, genetic disorders and autoimmune diseases, or as a side effect of medical therapy. These disorders affect the gland either directly (as with infections or autoimmune diseases) or as

neg: Adrenaline down-regulate its own synthesis. Abnormally elevated levels of adrenaline can occur in a variety of conditions, such as surreptitious epinephrine administration, pheochromocytoma, and other tumors of the sympathetic ganglia. Its action is terminated with reuptake into nerve terminal endings, some minute dilution, and metabolism by monoamine oxidase and catechol-"O"-methyl transferase. Extracts of the adrenal gland were first obtained by Polish physiologist Napoleon Cybulski in 1895. These extracts, which he called "nadnerczyna" ("adrenalin"), contained adrenaline and other catecholamines. American ophthalmologist William H. Bates discovered adrenaline's usage for eye surgeries prior to 20 April 1896. Japanese chemist Jokichi Takamine and his assistant

neg: Adrenal gland adrenal cortex and the inner medulla, both of which produce hormones. The adrenal cortex is the outermost layer of the adrenal gland. Within the cortex are three layers, called "zones". When viewed under a microscope each layer has a distinct appearance, and each has a different function. The adrenal cortex is devoted to production of hormones, namely aldosterone, cortisol, and androgens. The outermost zone of the adrenal cortex is the zona glomerulosa. It lies immediately under the fibrous capsule of the gland. Cells in this layer form oval groups, separated by thin strands of connective tissue from the fibrous capsule

neg: Feline hyperaldosteronism Feline hyperaldosteronism Feline hyperaldosteronism is a disease in cats. The symptoms are caused by abnormally high concentrations of the hormone aldosterone, which is secreted by the adrenal gland. The high concentrations of aldosterone may be due directly to a disorder of the adrenal gland (primary hyperadlosteronism), or due to something outside of the adrenal gland causing it to secrete excessive aldosterone (secondary hyperaldosteronism). Primary hyperaldosteronism (PHA) is a disorder of the adrenal cortex that causes increased circulating aldosterone levels. There are two types of PHA. One type is caused by a unilateral aldosterone-producing adenoma or adenocarcinoma. The other type, known