query: a type of hormone that the adrenal medulla secretes is a

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 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: 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: 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

pos: 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

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: 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: Homeostasis pressure in the arteries, causes the opposite reflex of constriction of the arterioles, and a speeding up of the heart rate (called tachycardia). If the drop in blood pressure is very rapid or excessive, the medulla oblongata stimulates the adrenal medulla, via "preganglionic" sympathetic nerves, to secrete epinephrine (adrenaline) into the blood. This hormone enhances the tachycardia and causes severe vasoconstriction of the arterioles to all but the essential organ in the body (especially the heart, lungs, and brain). These reactions usually correct the low arterial blood pressure (hypotension) very effectively. The plasma ionized calcium (Ca) concentration is very tightly

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 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: 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: Adrenaline the cytosol of the endocrine cells of the adrenal medulla (also known as chromaffin cells), it has been detected at low levels in both the heart and brain. The major physiologic triggers of adrenaline release center upon stresses, such as physical threat, excitement, noise, bright lights, and high or low ambient temperature. All of these stimuli are processed in the central nervous system. Adrenocorticotropic hormone (ACTH) and the sympathetic nervous system stimulate the synthesis of adrenaline precursors by enhancing the activity of tyrosine hydroxylase and dopamine β-hydroxylase, two key enzymes involved in catecholamine synthesis. ACTH also stimulates the adrenal cortex

pos: Aminophylline standing, but redissolves when a small amount of ethylenediamine is added. Insoluble in alcohol and in ether. Like other methylated xanthine derivatives, aminophylline is both a Aminophylline causes bronchodilation, diuresis, central nervous system and cardiac stimulation, and gastric acid secretion by blocking phosphodiesterase which increases tissue concentrations of cyclic adenosine monophosphate (cAMP) which in turn promotes catecholamine stimulation of lipolysis, glycogenolysis, and gluconeogenesis, and induces release of epinephrine from adrenal medulla cells. Note that diuresis is caused by an increase in cAMP which acts in the CNS to inhibit the release of antidiuretic hormone (arginine-vasopressin). Adenosine is an endogenous extracellular

pos: Enkephalin and the dynorphin gene. The proopiomelanocortin gene (POMC) also contains the met-enkephalin sequence on the N-terminus of beta-endorphin, but the endorphin peptide is not processed into enkephalin. Enkephalin is also considered a neuropeptide, which in the human body performs as an important signaling molecule in the brain. Enkephalins are found in high concentration in the brain as well as in the cells of adrenal medulla. In response to pain, norepinephrine, a hormone that is activated in fight-or-flight response is released along with endorphins. It has been shown that this polypeptide is linked to brain functioning during a stressful response, especially

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: 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: Adrenaline there being no direct neural connection from the sympathetic ganglia to the airway. The concept of the adrenal medulla and the sympathetic nervous system being involved in the flight, fight and fright response was originally proposed by Cannon. But the adrenal medulla, in contrast to the adrenal cortex, is not required for survival. In adrenalectomized patients hemodynamic and metabolic responses to stimuli such as hypoglycemia and exercise remain normal. One physiological stimulus to epinephrine secretion is exercise. This was first demonstrated using the denervated pupil of a cat as an assay, later confirmed using a biological assay on urine samples.

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: 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: 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: 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: Paroxysmal hypertension Paroxysmal hypertension Paroxysmal hypertension is episodic and volatile high blood pressure, which may be due to stress of any sort, or from a pheochromocytoma, a type of tumor involving the adrenal medulla. Patients with paroxysmal hypertension who test negative for pheochromocytoma are said to be suffering from a clinical entity called "pseudopheochromocytoma." This disorder is due to episodic dopamine discharge and has been observed predominantly in hypertensive women, that had episodes that shared similar characteristics of pheochromocytoma but testing proved negative and had ruled out the tumor. In patients with pseudopheochromocytoma dopamine was found to be significantly increased post-paroxysm. The

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: 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

neg: 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: 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: 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: 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: Sympathoadrenal system where they activate the release of adrenocorticotropic hormone (ACTH). The release of the adrenocorticotropic hormone is determined by the release of the corticotropin-releasing factor as the interruption of the corticotropin-releasing factor causes a weakening of the adrenocorticotropic hormone response. Adrenocorticotropic hormones bind to ACTH receptors on the cells within the adrenal medulla and adrenal cortex, causing a signal cascade within the adrenomedullary cell, ultimately releasing the neurotransmitter acetylcholine. The neurotransmitter acetylcholine causes the excitation of the nerves that innervate the skeletal muscles along with the muscles surrounding certain bodily systems such as the cardiovascular system and respiratory system, causing an

neg: Behavioral endocrinology body in its functions, and these would include a hormone such as Adrenaline. Cortisol is produced by the adrenal cortex above the kidneys and plays a major factor in neuroendocrinological behaviors. Cortisol helps in the regulation of metabolism and helps the body and brain respond to stress. Higher levels of cortisol to stressful situations promote: Adrenaline, or other wise known as Epineephrine) is released from the Adrenal medulla. Adrenaline is also released in response to the stimulation of the sympathetic nervous system or stress. Adrenal is known as the "fight or flight" hormone as rapidly rushes blood to muscles and

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: Anterior pituitary a role in stress response. Corticotropin releasing hormone (CRH) from the hypothalamus stimulates ACTH release in a cascading effect that ends with the production of glucocorticoids from the adrenal cortex. Hyperpituitarism is the condition where the pituitary secretes excessive amounts of hormones. This hypersecretion often results in the formation of a pituitary adenoma (tumour), which are benign apart from a tiny fraction. There are mainly three types of anterior pituitary tumors and their associated disorders. For example, acromegaly results from excessive secretion of growth hormone (GH) often being released by a pituitary adenoma. This disorder can cause disfigurement and possibly

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: Fluid balance the tubule in exchange for the sodium, which is reabsorbed. The activated renin–angiotensin system stimulates the zona glomerulosa of the adrenal cortex which in turn secretes the hormone aldosterone. This hormone stimulates the reabsorption of sodium ions from distal tubules and collecting ducts. Water in the tubular lumen cannot follow the sodium reabsorption osmotically, as this part of the kidney is impermeable to water; release of ADH (vasopressin) is required to increase expression of aquaporin channels in the cortical collecting duct, allowing reabsorption of water. Fluid balance Fluid balance is an aspect of the homeostasis of organisms in which the

neg: Adrenomedullin Adrenomedullin Adrenomedullin (ADM or AM) is a vasodilator peptide hormone of uncertain significance in human health and disease. It was initially isolated in 1993 from a pheochromocytoma, a tumor of the adrenal medulla: hence the name. In humans ADM is encoded by the "ADM" gene. ADM is a peptide expressed by all tissues, and found in the circulation. A similar peptide named adreomedullin2 was reported in rats in 2004 which exhibits a similar function. Adrenomedullin may function as a hormone in the circulation control because it is found in blood in a considerable concentration. It was initially identified as a

neg: Adrenomedullin effects and seems to confer advantages due to higher than normal bone mass, and reduced weight gain in older age. Adrenomedullin Adrenomedullin (ADM or AM) is a vasodilator peptide hormone of uncertain significance in human health and disease. It was initially isolated in 1993 from a pheochromocytoma, a tumor of the adrenal medulla: hence the name. In humans ADM is encoded by the "ADM" gene. ADM is a peptide expressed by all tissues, and found in the circulation. A similar peptide named adreomedullin2 was reported in rats in 2004 which exhibits a similar function. Adrenomedullin may function as a hormone

neg: 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

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: Adrenal gland before the beginning of puberty. The adrenal medulla is derived from neural crest cells, which come from the ectoderm layer of the embryo. These cells migrate from their initial position and aggregate in the vicinity of the dorsal aorta, a primitive blood vessel, which activates the differentiation of these cells through the release of proteins known as BMPs. These cells then undergo a second migration from the dorsal aorta to form the adrenal medulla and other organs of the sympathetic nervous system. Cells of the adrenal medulla are called chromaffin cells because they contain granules that stain with chromium salts,

neg: Hormone of the stomach and exocrine pancreas (the amounts of gastric juice and pancreatic juice) become the input of the small intestine, the small intestine secretes hormones to stimulate or inhibit the stomach and pancreas based on how busy it is. Regulation of hormone synthesis of gonadal hormones, adrenocortical hormones, and thyroid hormones is often dependent on complex sets of direct influence and feedback interactions involving the hypothalamic-pituitary-adrenal (HPA), -gonadal (HPG), and -thyroid (HPT) axes. Upon secretion, certain hormones, including protein hormones and catecholamines, are water-soluble and are thus readily transported through the circulatory system. Other hormones, including steroid and thyroid

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

neg: History of catecholamine research of muscarine elicited peristalsis. This peristalis was promptly abolished by electrical stimulation of the adrenals. The experiment has been called "the first indirect demonstration of the role of the adrenal medulla as an endocrine organ <and> actually a more sophisticated demonstration of the adrenal medullary function than the classic study of Oliver and Schäfer". While this may be true, Jacobj did not envisage a chemical signal secreted into the blood to influence distant organs, in other words a hormone, but nerves running from the adrenals to the gut, "Hemmungsbahnen für die Darmbewegung". George Oliver was a physician practicing in the

neg: Adrenal gland abundant mitochondria and a complex smooth endoplasmic reticulum. The innermost cortical layer, the zona reticularis, lies directly adjacent to the medulla. It produces androgens, mainly dehydroepiandrosterone (DHEA), DHEA sulfate (DHEA-S), and androstenedione (the precursor to testosterone) in humans. Its small cells form irregular cords and clusters, separated by capillaries and connective tissue. The cells contain relatively small quantities of cytoplasm and lipid droplets, and sometimes display brown lipofuscin pigment. The adrenal medulla is at the centre of each adrenal gland, and is surrounded by the adrenal cortex. The chromaffin cells of the medulla are the body's main source of the

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: Adrenal medulla fibers lead to them directly from the central nervous system. The adrenal medulla therefore affects available energy, heart rate, and metabolism. Recent research indicates that the adrenal medulla may receive input from higher-order cognitive centers in the prefrontal cortex as well as the sensory and motor cortices, providing credence to the idea that there are psychosomatic illnesses. Medullary cells are derived from the embryonic neural crest and, as such, are simply modified neurons. In particular, they are modified postganglionic cells of the autonomic nervous system that have lost their axons and dendrites, receiving innervation from corresponding preganglionic fibers. The cells

neg: Sheehan's syndrome antidiuretic hormone (ADH) hypersecretion, decreased free-water clearance by glucocorticoid deficiency (independent of ADH). The potassium level in these situations is normal, because adrenal production of aldosterone is not dependent on the pituitary. In the developed world it is a rare complication of pregnancy, usually occurring after excessive blood loss after delivery. The presence of disseminated intravascular coagulation (i.e., in amniotic fluid embolism or HELLP syndrome) also appears to be a factor in its development. Sheehan's syndrome is caused by damage to the pituitary, thereby causing a decrease in one or more hormones it normally secretes. Secondly, the anterior pituitary is

neg: Tachypsychia considers life-threatening, tachypsychia is believed to include numerous physical changes. Upon being stimulated by fear or anger, the adrenal medulla may automatically produce the hormone adrenaline directly into the blood stream. This can have various effects on various bodily systems, including: It is common for an individual to experience auditory exclusion or sensitivity. It is also common for individuals to experience an increased pain tolerance, loss of color vision, short term memory loss, decreased fine motor skills, decreased communication skills, or decreased coordination. The most common experience during tachypsychia is the feeling that time has either increased or slowed down,

neg: Chromaffin cell sides of the spinal cord toward the region just behind the dorsal aorta forming the two chains of sympathetic ganglia (Sympathetic chain). From these ganglia, the post synaptic sympathetic fibers will arise and extend toward their target organ. Some of these cells will migrate to the adrenal medulla to form sympathetic ganglia cells within the adrenal medulla (without postsynaptic sympathetic fibers). A tumor arising from these cells is called neuroblastoma. 2) Chromaffin cells (or pheochromocytes): These cells will migrate to the area adjacent to the sympathetic ganglia (hence the name paraganglia) and to the adrenal medulla where they will be

neg: Sympathoadrenal system sympathoadrenal system is to help the body regulate responses to environmental stimuli. These stimuli travel through the sympathetic nervous system by means of preganglionic nerve fibers that emerge from the thoracic spinal chord. Since both the sympathetic nerve fibers and adrenal medulla are part of the central nervous system (CNS), electrical impulses carried by the nervous system are converted to a chemical response in the adrenal gland. Chromaffin cells contained in the adrenal medulla act as postganglionic nerve fibers that release this chemical response into the blood as circulating messenger. The sympathoadrenal system can activate and discharge chemical messengers as

neg: Steroid hormone pathways are mediated by some type of steroid hormone receptor found at the plasma membrane. Ion channels, transporters, G-protein coupled receptors (GPCR), and membrane fluidity have all been shown to be affected by steroid hormones. Of these, GPCR linked proteins are the most common. For more information on these proteins and pathways, visit the steroid hormone receptor page. Steroid hormone A steroid hormone is a steroid that acts as a hormone. Steroid hormones can be grouped into two classes: corticosteroids (typically made in the adrenal cortex, hence "cortico-") and sex steroids (typically made in the gonads or placenta). Within those

neg: Neuroendocrine cell portal vessels to the pituitary cells where they may stimulate, inhibit, or maintain the function of a particular cell type. Neuroendocrine cell Neuroendocrine cells are cells that receive neuronal input (neurotransmitters released by nerve cells or neurosecretory cells) and, as a consequence of this input, release message molecules (hormones) to the blood. In this way they bring about an integration between the nervous system and the endocrine system, a process known as neuroendocrine integration. An example of a neuroendocrine cell is a cell of the adrenal medulla (innermost part of the adrenal gland), which releases adrenaline to the blood. The

neg: Corticotropin-releasing hormone receptor 2 more potent at stimulating CRHR2 beta than CRHR2 alpha and CRHR2 gamma, suggesting that the N-terminal sequence is involved in the ligand-receptor interaction. Corticotropin-releasing hormone receptor 2 Corticotropin-releasing hormone receptor 2 (CRHR2) is a protein, also known by the IUPHAR-recommended name CRF, that is encoded by the CRHR2 gene and occurs on the surfaces of some mammalian cells. CRF receptors are type 2 G protein-coupled receptors for corticotropin-releasing hormone (CRH) that are resident in the plasma membranes of hormone-sensitive cells. CRH, a peptide of 41 amino acids synthesized in the hypothalamus, is the principal neuroregulator of the hypothalamic-pituitary-adrenal axis, signaling

neg: Signal transduction nervous system and a hormone when secreted by the adrenal medulla. Some receptors such as HER2 are capable of ligand-independent activation when overexpressed or mutated. This leads to constituitive activation of the pathway, which may or may not be overturned by compensation mechanisms. In the case of HER2, which acts as a dimerization partner of other EGFRs, constituitive activation leads to hyperproliferation and cancer. The prevalence of basement membranes in the tissues of Eumetazoans means that most cell types require attachment to survive. This requirement has led to the development of complex mechanotransduction pathways, allowing cells to sense the stiffness

neg: Corticotropin-releasing hormone receptor 2 Corticotropin-releasing hormone receptor 2 Corticotropin-releasing hormone receptor 2 (CRHR2) is a protein, also known by the IUPHAR-recommended name CRF, that is encoded by the CRHR2 gene and occurs on the surfaces of some mammalian cells. CRF receptors are type 2 G protein-coupled receptors for corticotropin-releasing hormone (CRH) that are resident in the plasma membranes of hormone-sensitive cells. CRH, a peptide of 41 amino acids synthesized in the hypothalamus, is the principal neuroregulator of the hypothalamic-pituitary-adrenal axis, signaling via guanine nucleotide-binding proteins (G proteins) and downstream effectors such as adenylate cyclase. The CRF receptor is a multi-pass membrane protein with a

neg: Congenital adrenal hyperplasia due to 3β-hydroxysteroid dehydrogenase deficiency basic anatomy is present. Congenital adrenal hyperplasia due to 3β-hydroxysteroid dehydrogenase deficiency Congenital adrenal hyperplasia due to 3β-hydroxysteroid dehydrogenase deficiency is an uncommon form of congenital adrenal hyperplasia (CAH) resulting from a mutation in the gene for one of the key enzymes in cortisol synthesis by the adrenal gland, 3β-hydroxysteroid dehydrogenase (3β-HSD) type II (HSD3B2). As a result, higher levels of 17α-hydroxypregnenolone appear in the blood with adrenocorticotropic hormone (ACTH) challenge, which stimulates adrenal corticosteroid synthesis. There is a wide spectrum of clinical presentations of 3β-HSD CAH, from mild to severe forms. The uncommon severe form results from a complete

neg: Congenital adrenal hyperplasia due to 3β-hydroxysteroid dehydrogenase deficiency Congenital adrenal hyperplasia due to 3β-hydroxysteroid dehydrogenase deficiency Congenital adrenal hyperplasia due to 3β-hydroxysteroid dehydrogenase deficiency is an uncommon form of congenital adrenal hyperplasia (CAH) resulting from a mutation in the gene for one of the key enzymes in cortisol synthesis by the adrenal gland, 3β-hydroxysteroid dehydrogenase (3β-HSD) type II (HSD3B2). As a result, higher levels of 17α-hydroxypregnenolone appear in the blood with adrenocorticotropic hormone (ACTH) challenge, which stimulates adrenal corticosteroid synthesis. There is a wide spectrum of clinical presentations of 3β-HSD CAH, from mild to severe forms. The uncommon severe form results from a complete loss of enzymatic activity

neg: Tropic hormone Tropic hormone Tropic hormones are hormones that have other endocrine glands as their target. Most tropic hormones are produced and secreted by the anterior pituitary. The hypothalamus secretes tropic hormones that target the anterior pituitary, and the thyroid gland secretes thyroxine, which targets the hypothalamus and therefore can be considered a tropic hormone. The term "tropic" is from Ancient Greek τροπικός ("tropikós"), in the sense "of or pertaining to a turn or change", meaning "causing a change, affecting"; this is the same origin as "tropic" and "trope." This should not be confused with "trophic," as in similar-sounding trophic hormone –

neg: Neurohormone Neurohormone A neurohormone is any hormone produced and released by neuroendocrine cells (also called neurosecretory cells) into the blood. By definition of being hormones, they are secreted into the circulation for systemic effect, but they can also have a role of neurotransmitter or other roles such as autocrine (self) or paracrine (local) messenger. The hypothalamus produces releasing hormones and neurohypophysial hormones in specialized hypothalamic neurons which extend to the median eminence and posterior pituitary. The adrenal medulla produces adrenomedullary hormones in chromaffin cells, cells which are very similar in structure to post-synaptic sympathetic neurons, even though they are not neurons

neg: Adrenal gland affect the production of adrenocorticotropic hormone (ACTH) by the pituitary gland. This type of adrenal insufficiency usually does not affect the production of mineralocorticoids, which are under regulation of the renin–angiotensin system instead. Congenital adrenal hyperplasia is a congenital disease in which mutations of enzymes that produce steroid hormones result in a glucocorticoid deficiency and malfunction of the negative feedback loop of the HPA axis. In the HPA axis, cortisol (a glucocorticoid) inhibits the release of CRH and ACTH, hormones that in turn stimulate corticosteroid synthesis. As cortisol cannot be synthesized, these hormones are released in high quantities and stimulate

neg: Corticosterone as well as different types of memories themselves. Corticosterone Corticosterone, also known as 17-deoxycortisol and 11β,21-dihydroxyprogesterone, is a 21-carbon steroid hormone of the corticosteroid type produced in the cortex of the adrenal glands. It is of minor importance in humans, except in the very rare case of congenital adrenal hyperplasia due to 17 alpha-hydroxylase deficiency. In many species, including amphibians, reptiles, rodents and birds, corticosterone is a main glucocorticoid, involved in regulation of energy, immune reactions, and stress responses. However, in humans, cortisol is the primary glucocorticoid that is produced primarily in the zona fasciculata of the adrenal cortex. Corticosterone

neg: Corticosterone Corticosterone Corticosterone, also known as 17-deoxycortisol and 11β,21-dihydroxyprogesterone, is a 21-carbon steroid hormone of the corticosteroid type produced in the cortex of the adrenal glands. It is of minor importance in humans, except in the very rare case of congenital adrenal hyperplasia due to 17 alpha-hydroxylase deficiency. In many species, including amphibians, reptiles, rodents and birds, corticosterone is a main glucocorticoid, involved in regulation of energy, immune reactions, and stress responses. However, in humans, cortisol is the primary glucocorticoid that is produced primarily in the zona fasciculata of the adrenal cortex. Corticosterone has only weak glucocorticoid and mineralocorticoid potencies in

neg: Non-tropic hormone The Hypothalamic-pituitary-adrenal axis is a perfect example of this chain reaction. The reaction begins in the hypothalamus with a release of corticotropin-releasing hormone/factor (CRH/F; tropic). This stimulates the anterior pituitary and causes it to release Adrenocorticotropic hormone (ACTH; tropic) to the adrenal glands. Lastly, cortisol (non-tropic) is secreted from the adrenal glands and goes into the bloodstream where it can have more widespread effects on organs and tissues. Since cortisol is what finally reaches other tissues in the body, it is a non-tropic hormone. CRH an ACTH are tropic hormones because they act on the anterior pituitary gland and adrenal

neg: Adrenocortical hormone the pituitary gland or adrenal gland. In either case, treatment may rely on removal of the tumor or of the adrenal glands. Without the adrenal glands, the human body is unable to supply the hormones it produces and therefore requires hormone replacement therapy. Addison’s disease is an autoimmune disorder that affects the adrenal cortex such that it is unable to efficiently secrete hormones. The immune system specifically targets the cells of the adrenal cortex and destroys them, but Addison’s disease can also be caused by a severe infection such as tuberculosis. Some symptoms include hypoglycemia and decreased blood sodium levels

neg: Anticorticotropin Anticorticotropin An anticorticotropin, or anticorticotrophin, is a drug which opposes the actions of corticotropin-releasing hormone (CRH) and/or adrenocorticotropic hormone (ACTH) in relation to their stimulatory effects on the adrenal glands, or which otherwise suppresses steroid hormone production in the adrenal glands. They can be said to have anticorticotropic (or anticorticotrophic) effects, and are used to treat Cushing's syndrome, prostate cancer, hyperandrogenism, and other conditions. Some examples of anticorticotropins include the following: Conversely, drugs that stimulate CRH and/or ACTH secretion and/or activate adrenal steroidogenesis, such as antiglucocorticoids like mifepristone, antimineralocorticoids like spironolactone, and adrenal steroidogenesis inhibitors like ketoconazole, metyrapone, mitotane, and

neg: Adrenocorticotropic hormone Adrenocorticotropic hormone Adrenocorticotropic hormone (ACTH, also adrenocorticotropin, corticotropin) is a polypeptide tropic hormone produced by and secreted by the anterior pituitary gland. It is also used as a medication and diagnostic agent. ACTH is an important component of the hypothalamic-pituitary-adrenal axis and is often produced in response to biological stress (along with its precursor corticotropin-releasing hormone from the hypothalamus). Its principal effects are increased production and release of cortisol by the cortex of the adrenal gland. ACTH is also related to the circadian rhythm in many organisms. Deficiency of ACTH is a sign of secondary adrenal insufficiency (suppressed production of

neg: Sympathoadrenal system responses. Pheochromocytoma are rare tumors that secrete catecholamines and affect the sympathoadrenal system. They are typically found inside the adrenal medulla, but can also be present right outside the adrenal medulla in tissue. Symptoms include headaches, sweating, palpitations, hypertension, hypoglycemia, anxiety, weight loss, fever, nausea, and cardiovascular complications. Pheochromocytoma can be treated through blocking the effects of the secreted cathecholamines. Ideally, removal of the tumor is the preferred treatment and should be done in a timely manner for the best prognosis. On average, there is a delay of three years between initial symptoms and diagnosis because the tumors are hard

neg: 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

neg: Parathyroid hormone-related protein in function to the "normal" parathyroid hormone. When a tumor secretes PTHrP, this can lead to hypercalcemia. As this is sometimes the first sign of the malignancy, hypercalcemia caused by PTHrP is considered a paraneoplastic phenomenon. PTHR1 is responsible for most cases of humoral hypercalcemia of malignancy. PTHrP shares the same N-terminal end as parathyroid hormone and therefore it can bind to the same receptor, the Type I PTH receptor (PTHR1). PTHrP can simulate most of the actions of PTH including increases in bone resorption and distal tubular calcium reabsorption, and inhibition of proximal tubular phosphate transport. However, PTHrP is

neg: Corticotropin-releasing hormone receptor Corticotropin-releasing hormone receptor Corticotropin-releasing hormone receptors (CRHRs), also known as corticotropin-releasing factor receptors (CRFRs) are a G protein-coupled receptor family that binds corticotropin-releasing hormone (CRH). There are two receptors in the family, designated as type 1 and 2, each encoded by a separate gene ( and respectively). CRHRs are important mediators in the stress response. Cells in the anterior lobe of the pituitary gland known as corticotropes express the receptors and will secrete adrenocorticotropic hormone (ACTH) when stimulated. This binding of corticotropin releasing-hormone (CRH) activates the hypothalamic-pituitary-adrenal (HPA) axis, one of the two parts of the fight-or-flight response to stress.

neg: RVD-Hpα and its projections and in the adrenal medulla. RVD-Hpα also significantly potentiated the effects of CB2 receptor agonists, including the endocannabinoid 2-arachidonoyl glycerol (2-AG), for GTPγS binding and cAMP inhibition (5–10 fold). The putative precursor pepcan-23 was identified with pepcan-12 in brain, liver and kidney in mice. RVD-Hpα was increased upon endotoxemia and ischemia reperfusion damage where CB2 receptors play a protective role. The wide occurrence of this endogenous hormone-like CB2 receptor PAM, with unforeseen opposite allosteric effects on cannabinoid receptors, suggests its potential role in peripheral pathophysiological processes. RVD-Hpα RVD-Hpα is an endogenous neuropeptide found in human and mammalian

neg: Development of the endocrine system seven weeks of gestation, the adrenal cells are joined by sympathetic cells that originate from the neural crest to form the adrenal medulla. At the end of the eighth week, the adrenal glands have been encapsulated and have formed a distinct organ above the developing kidneys. At birth, the adrenal glands weight approximately eight to nine grams (twice that of the adult adrenal glands) and are 0.5% of the total body weight. At 25 weeks, the adult adrenal cortex zone develops and is responsible for the primary synthesis of steroids during the early postnatal weeks. The thyroid gland develops from

neg: Corticotropin-releasing hormone antagonist Corticotropin-releasing hormone antagonist A Corticotropin-Releasing Hormone Antagonist (CRH antagonist) is a specific type of receptor antagonist that blocks the receptor sites for Corticotropin-releasing hormone (also known as Corticotropin-releasing factor (CRF)), which synchronizes the behavioral, endocrine, autonomic, and immune responses to stress by controlling the hypothalamic-pituitary-adrenal axis (HPA Axis). CRH Antagonists thereby block the consequent secretions of ACTH and cortisol due to stress, among other effects. There are four subtypes of the CRH receptor known at present, defined as CRF-1, CRF-2a, CRF-2b, and CRF-2g. Three of these receptors are expressed only in the brain: CRF-1 in the cortex and cerebrum, CRF-2a

neg: Adrenal medulla the blood. Adrenaline composes about 85% of the released catecholamines, and noradrenaline the other 15%. Notable effects of adrenaline and noradrenaline include increased heart rate and blood pressure, blood vessel constriction in the skin and gastrointestinal tract, smooth muscle (bronchiole and capillary) dilation, and increased metabolism, all of which are characteristic of the fight-or-flight response. Release of catecholamines is stimulated by nerve impulses, and receptors for catecholamines are widely distributed throughout the body. Neoplasms include: The adrenal medulla may be poorly formed or absent in cases of absent adrenal gland. The deficiency in circulating catecholamines is mildly symptomatic due to

neg: 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

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: Oxytocin than peripheral levels. Outside the brain, oxytocin-containing cells have been identified in several diverse tissues, including in females in the corpus luteum and the placenta; in males in the testicles' interstitial cells of Leydig; and in both sexes in the retina, the adrenal medulla, the thymus and the pancreas. The finding of significant amounts of this classically "neurohypophysial" hormone outside the central nervous system raises many questions regarding its possible importance in these different tissues. The Leydig cells in some species have been shown to possess the biosynthetic machinery to manufacture testicular oxytocin "de novo", to be specific, in rats

neg: Maternal fetal stress transfer Cortisol is type of hormone called a glucocorticoid, which glucose usage in the body and tends to be activated during a fight-or-flight response. Cortisol is produced in the adrenal gland, whose activity is mediated by the hypothalamus and pituitary glands of the brain. Together, the collective signaling of the hypothalamus, pituitary gland, and adrenal gland is known as the hypothalamo-pituitary-adrenal (HPA) axis. During a period of psychosocial stress, cortisol is released, leading to physiological manifestations of stress such as increased maternal blood pressure (MBP) and maternal heart rate (MHR). In the case of a pregnant woman, the release of cortisol

neg: Adrenal gland glands are first detectable after the sixth week of development. Adrenal cortex tissue is derived from the intermediate mesoderm. It first appears 33 days after fertilisation, shows steroid hormone production capabilities by the eighth week and undergoes rapid growth during the first trimester of pregnancy. The fetal adrenal cortex is different from its adult counterpart, as it is composed of two distinct zones: the inner "fetal" zone, which carries most of the hormone-producing activity, and the outer "definitive" zone, which is in a proliferative phase. The fetal zone produces large amounts of adrenal androgens (male sex hormones) that are used

neg: Alpha-3 beta-4 nicotinic receptor Alpha-3 beta-4 nicotinic receptor The alpha-3 beta-4 nicotinic receptor, also known as the α3β4 receptor and the ganglion-type nicotinic receptor, is a type of nicotinic acetylcholine receptor, consisting of α3 and β4 subunits. It is located in the autonomic ganglia and adrenal medulla, where activation yields post- and/or presynaptic excitation, mainly by increased Na and K permeability. As with other nicotinic acetylcholine receptors, the α3β4 receptor is pentameric [(α3)(β4) where m + n = 5]. The exact subunit stoichiometry is not known and it is possible that more than one functional α3β4 receptor assembles in vivo with varying subunit stoichiometries.

neg: Alpha-3 beta-4 nicotinic receptor Alpha-3 beta-4 nicotinic receptor The alpha-3 beta-4 nicotinic receptor, also known as the α3β4 receptor and the ganglion-type nicotinic receptor, is a type of nicotinic acetylcholine receptor, consisting of α3 and β4 subunits. It is located in the autonomic ganglia and adrenal medulla, where activation yields post- and/or presynaptic excitation, mainly by increased Na and K permeability. As with other nicotinic acetylcholine receptors, the α3β4 receptor is pentameric [(α3)(β4) where m + n = 5]. The exact subunit stoichiometry is not known and it is possible that more than one functional α3β4 receptor assembles in vivo with varying subunit stoichiometries.

neg: Glucocorticoid hormone and pituitary adrenocorticotropic hormone. With prolonged suppression, the adrenal glands atrophy (physically shrink), and can take months to recover full function after discontinuation of the exogenous glucocorticoid. During this recovery time, the patient is vulnerable to adrenal insufficiency during times of stress, such as illness. While suppressive dose and time for adrenal recovery vary widely, clinical guidelines have been devised to estimate potential adrenal suppression and recovery, to reduce risk to the patient. The following is one example: Glucocorticoid Glucocorticoids are a class of corticosteroids, which are a class of steroid hormones. Glucocorticoids are corticosteroids that bind to the

neg: Addison's disease glandular damage). Autoimmune adrenalitis is the most common cause of Addison's disease in the industrialized world. Autoimmune destruction of the adrenal cortex is caused by an immune reaction against the enzyme 21-hydroxylase (a phenomenon first described in 1992). This may be isolated or in the context of autoimmune polyendocrine syndrome (APS type 1 or 2), in which other hormone-producing organs, such as the thyroid and pancreas, may also be affected. Adrenal destruction is also a feature of adrenoleukodystrophy, and when the adrenal glands are involved in metastasis (seeding of cancer cells from elsewhere in the body, especially lung), hemorrhage (e.g.,

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: Development of the endocrine system Development of the endocrine system The fetal endocrine system is one of the first systems to develop during prenatal development. The fetal adrenal cortex can be identified within four weeks of gestation. The adrenal cortex originates from the thickening of the intermediate mesoderm. At five to six weeks of gestation, the mesonephros differentiates into a tissue known as the gonadal ridge. The gonadal ridge produces the steroidogenic cells for both the gonads and the adrenal cortex. The adrenal medulla is derived from ectodermal cells. Cells that will become adrenal tissue move retroperitoneally to the upper portion of the mesonephros. At

neg: Adrenal gland of 1 case per million per year. Pheochromocytomas are tumors of the adrenal medulla that arise from chromaffin cells. They can produce a variety of nonspecific symptoms, which include headaches, sweating, anxiety and palpitations. Common signs include hypertension and tachycardia. Surgery, especially adrenal laparoscopy, is the most common treatment for small pheochromocytomas. Bartolomeo Eustachi, an Italian anatomist,is credited with the first description of the adrenal glands in 1563-4. However, these publications were part of the papal library and did not receive public attention, which was first received with Caspar Bartholin the Elder's illustrations in 1611. The adrenal glands are named

neg: Anticorticotropin aminoglutethimide, have "corticotropic" or "procorticotropic" effects. Anticorticotropins are analogous to antigonadotropins and procorticotropins are analogous to progonadotropins. Anticorticotropin An anticorticotropin, or anticorticotrophin, is a drug which opposes the actions of corticotropin-releasing hormone (CRH) and/or adrenocorticotropic hormone (ACTH) in relation to their stimulatory effects on the adrenal glands, or which otherwise suppresses steroid hormone production in the adrenal glands. They can be said to have anticorticotropic (or anticorticotrophic) effects, and are used to treat Cushing's syndrome, prostate cancer, hyperandrogenism, and other conditions. Some examples of anticorticotropins include the following: Conversely, drugs that stimulate CRH and/or ACTH secretion and/or activate adrenal steroidogenesis,

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: Hypoaldosteronism is so large that it is almost impossible to prevent eventual collapse and death unless mineralocorticoid treatment is also instituted. Hypoaldosteronism Hypoaldosteronism is an endocrinological disorder characterized decreased levels of the hormone aldosterone. Similarly, isolated hypoaldosteronism is the condition of having lowered aldosterone without corresponding changes in cortisol. (The two hormones are both produced by the adrenals.) There are several causes for this condition, including adrenal insufficiency, congenital adrenal hyperplasia, and some medications such as certain diuretics, NSAIDs, and ACE inhibitors. Hypoaldosteronism may result in hyperkalemia and is the cause of 'type 4 renal tubular acidosis', sometimes referred to as

neg: Adrenal insufficiency 1992). This may be isolated or in the context of autoimmune polyendocrine syndrome (APS type 1 or 2), in which other hormone-producing organs, such as the thyroid and pancreas, may also be affected. Adrenal destruction is also a feature of adrenoleukodystrophy (ALD), and when the adrenal glands are involved in metastasis (seeding of cancer cells from elsewhere in the body, especially lung), hemorrhage (e.g. in Waterhouse-Friderichsen syndrome or antiphospholipid syndrome), particular infections (tuberculosis, histoplasmosis, coccidioidomycosis), or the deposition of abnormal protein in amyloidosis. Hyponatremia can be caused by glucocorticoid deficiency. Low levels of glucocorticoids leads to systemic hypotension (one of

neg: Peptide hormone growth hormone, which acts on bone, muscle, and the liver. The posterior pituitary gland secretes antidiuretic hormone, also called vasopressin, and oxytocin. The parathyroid gland secretes parathyroid hormone, the main hormone responsible for regulating serum calcium and phosphorus levels. Peptide hormones are also produced by many different organs and tissues, including the heart (atrial-natriuretic peptide (ANP) or atrial natriuretic factor (ANF)) and pancreas (glucagon, insulin and somatostatin), the gastrointestinal tract (cholecystokinin, gastrin), and adipose tissue stores (leptin). Peptide hormone Peptide hormones or protein hormones are hormones whose molecules are peptides or proteins, respectively. The latter have longer amino acid chain

neg: Adrenal insufficiency cortisol) or adrenal destruction (disease processes leading to glandular damage). Use of high-dose steroids for more than a week begins to produce suppression of the person's adrenal glands because the exogenous glucocorticoids suppress release of hypothalamic corticotropin-releasing hormone (CRH) and pituitary adrenocorticotropic hormone (ACTH). With prolonged suppression, the adrenal glands atrophy (physically shrink), and can take months to recover full function after discontinuation of the exogenous glucocorticoid. During this recovery time, the person is vulnerable to adrenal insufficiency during times of stress, such as illness, due to both adrenal atrophy and suppression of CRH and ACTH release. Use of steroids

neg: Behavioral endocrinology throughout your body: The production of too much Thyroxine and triiodothyronine result in Hyperthyroidism. Some potential side effects are: The production of too little thyroxine and triodothyronine results in Hypothyrodism. Some potential side effects are: The 2 adrenal glands are located on the top of the kidney and have two distinct sections. The outer region called the outer part which is called the adrenal cortex. The adrenal cortex produce the hormones that are essential for life such as Cortisol and Aldosterone. The inner section, or the Adrenal medulla produce hormones that are not essential for life itself but assist the

neg: Amphenone B iodide by the thyroid gland. Amphenone B was first synthesized in 1950 and is a diphenylmethane derivative that was derived from the insecticide 2,2-di("p"-chlorophenyl)-1,1-dichloroethane (p,p'-DDD), which in 1949 had been found to selectively induce adrenal atrophy. In contrast to p,p'-DDD, which has direct cytotoxic effects on the adrenal glands via an unknown mechanism, amphenone B does not have cytotoxic effects, and instead causes adrenal and thyroid gland hypertrophy due to respective inhibition of corticosteroid and thyroxine biosynthesis, subsequent loss of negative feedback on the hypothalamic-pituitary-adrenal and hypothalamic-pituitary-thyroid axes, and consequent hypersecretion of adrenocorticotropic hormone (ACTH) and thyroid-stimulating hormone (TSH) from

neg: Cushing's syndrome and lower back. Cushing’s syndrome includes all the causes of increased cortisol leading to the diseased state. Cushing’s disease is a specific type of Cushing’s syndrome caused by a pituitary tumor leading to excessive production of ACTH (adrenocorticotropic hormone). Excessive ACTH stimulates the adrenal cortex to produce high levels of cortisol, producing the disease state. Cushing's disease due to excess ACTH may also result in hyperpigmentation. This is due to Melanocyte-Stimulating Hormone production as a byproduct of ACTH synthesis from Pro-opiomelanocortin (POMC). Alternatively, it is proposed that the high levels of ACTH, β-lipotropin, and γ-lipotropin, which contain weak MSH function,

neg: Corticotropin-releasing factor family in the paraventricular nucleus of the mammalian hypothalamus that regulates the release of corticotropin (ACTH) from the pituitary gland. The paraventricular nucleus transports CRH to the anterior pituitary, stimulating adrenocorticotropic hormone (ACTH) release via CRH type 1 receptors, thereby activating the hypothalamic-pituitary-adrenal axis (HPA) and, thus, glucocorticoid release. CRH is evolutionary-related to a number of other active peptides. Urocortin acts "in vitro" to stimulate the secretion of adrenocorticotropic hormone. Urotensin is found in the teleost caudal neurosecretory system and may play a role in osmoregulation and as a corticotropin-releasing factor. Urotensin-I is released from the urophysis of fish, and produces

neg: ACTH stimulation test ACTH stimulation test The ACTH test (also called the cosyntropin, tetracosactide, or Synacthen test) is a medical test usually ordered and interpreted by endocrinologists to assess the functioning of the adrenal glands stress response by measuring the adrenal response to adrenocorticotropic hormone (ACTH; corticotropin) or another corticotropic agent such as tetracosactide (cosyntropin, tetracosactrin; Synacthen) or alsactide (Synchrodyn). ACTH is a hormone produced in the anterior pituitary gland that stimulates the adrenal glands to release cortisol, dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEA-S), and aldosterone. During the test, a small amount of synthetic ACTH is injected, and the amount of cortisol (and sometimes

neg: Cortisol of three layers comprising the adrenal cortex. The cortex forms the outer "bark" of each adrenal gland, situated atop the kidneys. The release of cortisol is controlled by the hypothalamus, a part of the brain. The secretion of corticotropin-releasing hormone by the hypothalamus triggers cells in the neighboring anterior pituitary to secrete another hormone, the adrenocorticotropic hormone (ACTH), into the vascular system, through which blood carries it to the adrenal cortex. ACTH stimulates the synthesis of cortisol and other glucocorticoids, mineralocorticoids, and dehydroepiandrosterone. Normal values indicated in the following tables pertain to humans (normal levels vary among species). Measured cortisol

neg: Adrenocorticotropic hormone a short period of time, ACTH is cleaved into α-melanocyte-stimulating hormone (α-MSH) and CLIP, a peptide with unknown activity in humans. Human ACTH has a molecular weight of 4,540 atomic mass units (Da). ACTH stimulates secretion of glucocorticoid steroid hormones from adrenal cortex cells, especially in the zona fasciculata of the adrenal glands. ACTH acts by binding to cell surface ACTH receptors, which are located primarily on adrenocortical cells of the adrenal cortex. The ACTH receptor is a seven-membrane-spanning G protein-coupled receptor. Upon ligand binding, the receptor undergoes conformation changes that stimulate the enzyme adenylyl cyclase, which leads to an

neg: Transthyretin Transthyretin Transthyretin (TTR or TBPA) is a transport protein in the serum and cerebrospinal fluid that carries the thyroid hormone thyroxine (T) and retinol-binding protein bound to retinol. This is how transthyretin gained its name: "transports thyroxine and retinol". The liver secretes transthyretin into the blood, and the choroid plexus secretes TTR into the cerebrospinal fluid. TTR was originally called prealbumin (or thyroxine-binding prealbumin) because it ran faster than albumin on electrophoresis gels. It functions in concert with two other thyroid hormone-binding proteins in the serum: In cerebrospinal fluid TTR is the primary carrier of T. TTR also acts as