query: which division of the and stimulates the secretion of hormones by the adrenal medulla

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: 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

pos: Adrenaline to release cortisol, which increases the expression of PNMT in chromaffin cells, enhancing adrenaline synthesis. This is most often done in response to stress. The sympathetic nervous system, acting via splanchnic nerves to the adrenal medulla, stimulates the release of adrenaline. Acetylcholine released by preganglionic sympathetic fibers of these nerves acts on nicotinic acetylcholine receptors, causing cell depolarization and an influx of calcium through voltage-gated calcium channels. Calcium triggers the exocytosis of chromaffin granules and, thus, the release of adrenaline (and noradrenaline) into the bloodstream. Unlike many other hormones adrenaline (as with other catecholamines) does not exert negative feedback to

pos: Neuroendocrine cell 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 adrenal medullary cells are controlled by the sympathetic division of the autonomic nervous system. These cells are modified postganglionic neurons.

pos: Adrenal gland increasing the levels of tyrosine hydroxylase and PNMT. Catecholamine release is stimulated by the activation of the sympathetic nervous system. Splanchnic nerves of the sympathetic nervous system innervate the medulla of the adrenal gland. When activated, it evokes the release of catecholamines from the storage granules by stimulating the opening of calcium channels in the cell membrane. Cells in zona reticularis of the adrenal glands produce male sex hormones, or androgens, the most important of which is DHEA. In general, these hormones do not have an overall effect in the male body, and are converted to more potent androgens such

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: 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: 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: 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: 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: 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

pos: Muscarinic acetylcholine receptor is supplied by cholinergic preganglionic sympathetic fibers: acetylcholine is the neurotransmitter utilized at this synapse. The chromaffin cells of the adrenal medulla act as "modified neurons", releasing adrenaline and noradrenaline into the bloodstream as hormones instead of as neurotransmitters. The other postganglionic fibers of the peripheral autonomic system belong to the parasympathetic division; all are cholinergic fibers, and use acetylcholine as the neurotransmitter. Another role for these receptors is at the junction of the innervated tissues and the postganglionic neurons in the parasympathetic division of the autonomic nervous system. Here acetylcholine is again used as a neurotransmitter, and "muscarinic" receptors

pos: Neurohormone the pars nervosa of the posterior pituitary, where they are stored and released into the systemic circulation. The synthesis, control, and release of those hormones is co-regulated by hormonal, local and synaptic signals. Neurohypophysial hormones include: This is through this pathway that the vast majority of oxytocin and vasopressin hormones reach the systemic circulation. Adrenomedullary hormones are catecholamines secreted from the adrenal medulla by chromaffin cells, neurosecretory cells connected to the central nervous system. The synthesis, storage (in chromaffin cells) and release of catecholamines is co-regulated by synaptic input from their respective pre-synaptic sympathetic neurons, as well as hormonal and

pos: Regulation of gastric function absorbed by the duodenum stimulate acid secretion by unknown mechanisms. 4.) Osmolarity due to products of digestion stimulate acid secretion The acid and semi-digested fats in the duodenum trigger the enterogastric reflex – the duodenum sends inhibitory signals to the stomach by way of the enteric nervous system, and sends signals to the medulla that (1) inhibit the vagal nuclei, thus reducing vagal stimulation of the stomach, and (2) stimulate sympathetic neurons, which send inhibitory signals to the stomach. Chyme also stimulates duodenal enteroendocrine cells to release secretin and cholecystokinin. They primarily stimulate the pancreas and gall bladder, but also

pos: 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

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: 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: 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: 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: 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: 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,

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: 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: Acute stress reaction of glucose released by the liver. The onset of an acute stress response is associated with specific physiological actions in the sympathetic nervous system, both directly and indirectly through the release of adrenaline and to a lesser extent noradrenaline from the medulla of the adrenal glands. These catecholamine hormones facilitate immediate physical reactions by triggering increases in heart rate and breathing, constricting blood vessels. An abundance of catecholamines at neuroreceptor sites facilitates reliance on spontaneous or intuitive behaviors often related to combat or escape. Normally, when a person is in a serene, unstimulated state, the "firing" of neurons in the

pos: 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: Pituitary apoplexy The pituitary gland consists of two parts, the anterior (front) and posterior (back) pituitary. Both parts release hormones that control numerous other organs. In pituitary apoplexy, the main initial problem is a lack of secretion of adrenocorticotropic hormone (ACTH, corticotropin), which stimulates the secretion of cortisol by the adrenal gland. This occurs in 70% of those with pituitary apoplexy. A sudden lack of cortisol in the body leads to a constellation of symptoms called "adrenal crisis" or "Addisonian crisis" (after a complication of Addison's disease, the main cause of adrenal dysfunction and low cortisol levels). The main problems are low

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: 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

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: Cortisol body post stress. This can be evidenced through a decrease in systolic and diastolic blood pressures and decreased salivary cortisol level after treatment with ascorbic acid. Cortisol is synthesized from cholesterol. Synthesis takes place in the zona fasciculata of the adrenal cortex. (The name cortisol is derived from cortex.) While the adrenal cortex also produces aldosterone (in the zona glomerulosa) and some sex hormones (in the zona reticularis), cortisol is its main secretion in humans and several other species. (However, in cattle, corticosterone levels may approach or exceed cortisol levels.). The medulla of the adrenal gland lies under the cortex,

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: 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;

neg: Choh Hao Li he was elected as Academician of Academia Sinica, Republic of China. Li spent his entire academic career studying the pituitary-gland hormones. In collaboration with various co-workers, he isolated several protein hormones, including adrenocorticotropic hormone (ACTH), which stimulates the adrenal cortex to increase its secretion of corticoids. In 1956, Li and his group showed that ACTH consists of 39 amino acids arranged in a specific order, and that the whole chain of the natural hormone is not necessary for its action. He isolated another pituitary hormone called melanocyte-stimulating hormone (MSH) and found that not only does this hormone produce some effects

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: 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: 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: 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: Regulation of gastric function secretion (via parietal and G cells). Sensory stimuli from food activate dorsal motor nucleus of vagus nerve in the medulla (activating the parasympathetic nervous system). Insulin induced hypoglycemia also stimulates the vagus nerve. This results in four distinct physiological events. 1.) In the body of the stomach, the vagal postganglionic muscarinic nerves release acetylcholine(ACh) which stimulates parietal cell H+ secretion. 2.) In the lamina propria of the body of the stomach the ACh released from the vagal endings triggers histamine secretion from ECL cells. Histamine also stimulates H+ secretion from parietal cells. 3.) In the antrum, peptidergic postganglionic parasympathetic vagal

neg: Extended female sexuality extended female sexuality has evolved as a by-product of an adaptation in females that increases the levels of adrenal hormones. He proposed that secretion of higher levels of adrenal hormones were initially selected in women in order to increase endurance for walking or running. This hypothesis suggests that the larger adrenal glands may have contributed to the development of extended female sexuality as they are also the main source of 'libido hormones', which increase the female's sexual drive. Thus, extended sexuality is little to do with sexual behavior, or evolutionary advantage, but rather it is just a by-product of hormones.

neg: Regulation of gastric function acid secretion during these times is regulated by body weight, individual, number of parietal cells, and time of day. Acid secretion is lowest in the morning before awakening and highest at night. The cephalic phase is the stage in which the stomach responds to the mere sight, smell, taste, or thought of food. About 30% of total acid secretion occurs before food enters the stomach. These sensory and mental inputs converge on the hypothalamus, which relays signals to the medulla oblongata. Vagus nerve fibers from the medulla stimulate the parasympathetic nervous system of the stomach which, in turn, stimulates gastric

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: 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: Hypothalamic disease signals to the pituitary to release thyroid-stimulating hormone (TSH), which then stimulates the thyroid to secrete T and T thyroid hormones. Secondary hypothyroidism occurs when TSH secretion from the pituitary is impaired, whereas tertiary hypothyroidism is the deficiency or inhibition of TRH. Thyroid hormones are responsible for metabolic activity. Insufficient production of the thyroid hormones result in suppressed metabolic activity and weight gain. Hypothalamic disease may therefore have implications for obesity. Growth hormone-releasing hormone (GHRH) is another releasing factor secreted by the hypothalamus. GHRH stimulates the pituitary gland to secrete growth hormone (GH), which has various effects on body growth

neg: Hypothalamic–pituitary–thyroid axis these animals. The pituitary gland secretes thyrotropin (TSH; Thyroid Stimulating Hormone) that stimulates the thyroid to secrete thyroxine (T4) and, to a lesser degree, triiodothyronine (T3). The major portion of T3, however, is produced in peripheral organs, e.g. liver, adipose tissue, glia and skeletal muscle by deiodination from circulating T4. Deiodination is controlled by numerous hormones and nerval signals including TSH, vasopressin and catecholamines. Both peripheral thyroid hormones (iodothyronines) inhibit thyrotropin secretion from the pituitary (negative feedback). Consequently, equilibrium concentrations for all hormones are attained. TSH secretion is also controlled by thyrotropin releasing hormone (thyroliberin, TRH), whose secretion itself is

neg: Adrenal gland glucocorticoids cortisol and corticosterone are synthesized in the zona fasciculata; their functions include the regulation of metabolism and immune system suppression. The innermost layer of the cortex, the zona reticularis, produces androgens that are converted to fully functional sex hormones in the gonads and other target organs. The production of steroid hormones is called steroidogenesis, and involves a number of reactions and processes that take place in cortical cells. The medulla produces the catecholamines adrenaline and noradrenaline, which function to produce a rapid response throughout the body in stress situations. A number of endocrine diseases involve dysfunctions of the adrenal

neg: Adrenal insufficiency Adrenal insufficiency Adrenal insufficiency is a condition in which the adrenal glands do not produce adequate amounts of steroid hormones, primarily cortisol; but may also include impaired production of aldosterone (a mineralocorticoid), which regulates sodium conservation, potassium secretion, and water retention. Craving for salt or salty foods due to the urinary losses of sodium is common. Addison's disease and congenital adrenal hyperplasia can manifest as adrenal insufficiency. If not treated, adrenal insufficiency may result in severe abdominal pains, vomiting, profound muscle weakness and fatigue, depression, extremely low blood pressure (hypotension), weight loss, kidney failure, changes in mood and personality, and

neg: Adrenal gland compounds that have a structure made of a catechol group and an amine group. The adrenal glands are responsible for most of the adrenaline that circulates in the body, but only for a small amount of circulating noradrenaline. These hormones are released by the adrenal medulla, which contains a dense network of blood vessels. Adrenaline and noradrenaline act at adrenoreceptors throughout the body, with effects that include an increase in blood pressure and heart rate. actions of adrenaline and noradrenaline are responsible for the fight or flight response, characterised by a quickening of breathing and heart rate, an increase in

neg: Zona reticularis ovaries to produce testosterone and the estrogens respectively. ACTH partially regulates adrenal androgen secretion, also CRH. In humans the reticularis layer does contain 17 alpha-hydroxylase; this hydroxylates pregnenolone, which is then converted to cortisol by a mixed function oxidase. In rodents, the lack of 17alpha-hydroxylase results in the synthesis of corticosterone instead of cortisol as in the human. Zona reticularis The zona reticularis is the innermost layer of the adrenal cortex, lying deep to the zona fasciculata and superficial to the adrenal medulla. The cells are arranged cords that project in different directions giving a net-like appearance (L. reticulum -

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: Regulation of gastric function Somatostatin inhibits gastrin release from G cells. Reduced gastrin secretion reduces acid secretion. 5-10% of gastric secretion occurs during this phase. The intestinal phase is a stage in which the duodenum responds to arriving chyme and moderates gastric activity through hormones and nervous reflexes. The duodenum initially enhances gastric secretion, but soon inhibits it. Presence of partially digested proteins and amino acids in the duodenum stimulates acid secretion in the stomach by three methods: 1.) Peptones stimulate duodenal G Cells to secrete gastrin. 2.) Peptones stimulate an unknown endocrine cell to release an additional humoral signal, "enterooxytonin". 3.) Amino Acids

neg: Adrenaline of epinephrine can be seen in autonomic neuropathy or following adrenalectomy. Failure of the adrenal cortex, as with Addisons disease, can suppress epinephrine secretion as the activity of the synthesing enzyme, phenylethanolamine-"N"-methyltransferase, depends on the high concentration of cortisol that drains from the cortex to the medulla. In 1901, Jokichi Takamine patented a purified extract from the adrenal glands, and called it "adrenalin" (from the Latin for "on top of the kidneys" ("ad" and "renal"), which was trademarked by Parke, Davis & Co in the US. The British Approved Name and European Pharmacopoeia term for this drug is hence "adrenaline".

neg: Cortisone in the adrenal gland (suprarenal) to become any one of many steroid hormones. One end-product of this pathway is cortisol. For cortisol to be released from the adrenal gland, a cascade of signaling occurs. Corticotropin-releasing hormone released from the hypothalamus stimulates corticotrophs in the anterior pituitary to release ACTH, which relays the signal to the adrenal cortex. Here, the zona fasciculata and zona reticularis, in response to ACTH, secrete glucocorticoids, in particular cortisol. In the peripheral tissues, cortisol is converted to cortisone by the enzyme 11-beta-steroid dehydrogenase. Cortisone has marginally reduced glucocorticoid activity compared to cortisol (80-90%), and thus, cortisone

neg: Non-tropic hormone glands, respectively, both of which are endocrine glands. Non-tropic hormones are thus often the last piece of a larger process and chain of hormone secretion. Both tropic and non-tropic hormones are necessary for proper endocrine function. For example, if ACTH (Adrenocorticotropin hormone; a tropic hormone) is inhibited, cortisol can no longer be released because the chain reaction has been interrupted. Some examples of non-tropic hormones are: Most endocrine glands, such as the gonads, pancreas, and adrenal glands, produce non-tropic hormones. Those released from the pituitary gland in the brain include: Non-tropic hormone Non-tropic hormones are hormones that directly stimulate target

neg: Kisspeptin of GPR54 is not discernable in pyramidal cells, but has high levels of expression in the granule cell layer. It is known to be found in specific nuclei and neurons. The neuropeptide kisspeptin plays an important role in reproduction, but also stimulates aldosterone secretion from the adrenal cortex. Kisspeptin is distributed from the adrenal cortex and it is transcribed in the neocortex. The exact nature of the expression of kisspeptins in human adrenal glands unfortunately has not been fully clarified yet and remains a large topic of research among many scientists. Kisspeptin is a product of the KISS1 gene which

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: Pancreatic polypeptide in anorexia nervosa. In addition, peripheral administration of PP has been shown to decrease food intake in rodents. PP is secreted by PP pancreatic cells of Langerhans islets. It stimulates the gastric juice secretion, but inhibits the gastric secretion induced by pentagastrine. It is the antagonist of cholecystokinin and inhibits the pancreatic secretion which is stimulated by cholecystokinin. On fasting, PP seric concentration is 80 pg/ml; after the meal, it rises up from 8 to 10 times more; glucose and fats also induce PP's level increase, but on parenteral introduction of those substances, the level of hormones doesn't change. The

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: Hypothalamus this is sometimes called a "hypothalamic fever". However, it is more common for such damage to cause abnormally low body temperatures. The hypothalamus contains neurons that react strongly to steroids and glucocorticoids – (the steroid hormones of the adrenal gland, released in response to ACTH). It also contains specialized glucose-sensitive neurons (in the arcuate nucleus and ventromedial hypothalamus), which are important for appetite. The preoptic area contains thermosensitive neurons; these are important for TRH secretion. Oxytocin secretion in response to suckling or vagino-cervical stimulation is mediated by some of these pathways; vasopressin secretion in response to cardiovascular stimuli arising from

neg: Enteroendocrine cell somatostatin Gastric enteroendocrine cells are found in the gastric glands, mostly at their base. The G cells secrete gastrin, post-ganglionic fibers of the vagus nerve can release gastrin-releasing peptide during parasympathetic stimulation to stimulate secretion. Enterochromaffin-like cells are enteroendocrine and neuroendocrine cells also known for their similarity to chromaffin cells secreting histamine, which stimulates G cells to secrete gastrin. Other hormones produced include cholecystokinin, somatostatin, vasoactive intestinal peptide, substance P, alpha and gamma-endorphin. Pancreatic enteroendocrine cells are located in the islets of Langerhans and produce most importantly the hormones insulin and glucagon. The autonomous nervous system strongly regulates their secretion,

neg: Hypothalamic–pituitary–adrenal axis the portal blood vessel system of the hypophyseal stalk and vasopressin is transported by axonal transport to the posterior pituitary gland. There, CRH and vasopressin act synergistically to stimulate the secretion of stored ACTH from corticotrope cells. ACTH is transported by the blood to the adrenal cortex of the adrenal gland, where it rapidly stimulates biosynthesis of corticosteroids such as cortisol from cholesterol. Cortisol is a major stress hormone and has effects on many tissues in the body, including the brain. In the brain, cortisol acts on two types of receptor – mineralocorticoid receptors and glucocorticoid receptors, and these are

neg: Endocrine gland gonads in both sexes. FSH stimulates sex cell production; LH stimulates gonadal hormone production. Gonadotropin levels rise in response to gonadotropin-releasing hormone (GnRH). Negative feedback of gonadal hormones inhibits gonadotropin release. Prolactin (PRL) promotes milk production in human females. Its secretion is prompted by prolactin-releasing hormone (PRH) and inhibited by prolactin-inhibiting hormone (PIH). The neurohypophysis stores and releases two hypothalamic hormones: The thyroid gland is located at the front of the neck, in front of the thyroid cartilage, and is shaped like a butterfly, with two wings connected by a central . Thyroid tissue consists of follicles with stored protein

neg: Neuroendocrinology its product?" and "how is information encoded in electrical activity?"[It appears that this is a primary source observation.] The pituitary gland is divided into two sections: the anterior pituitary and the posterior pituitary. The hypothalamus controls the anterior pituitary's hormone secretion by sending trophic hormones down the hypothalamohypophysial portal system. For example, thyrotropin-releasing hormone stimulates the secretion of thyroid-stimulating hormone by the anterior pituitary. The posterior pituitary is innervated by the hypothalamus; the hormones oxytocin and vasopressin are synthesized by neuroendocrine cells in the hypothalamus and stored at the nerves' ends in the posterior pituitary. They are secreted directly into

neg: Adrenopause is analogous to andropause in men and menopause in women, the abrupt or gradual decline in production of sex hormones from the gonads with age. DHEA can be supplemented or taken as a medication in the form of prasterone to replace adrenal androgens later in life if it is desired. Some clinical studies have found benefits of DHEA supplementation in the elderly and people with adrenal insufficiency. Adrenopause Adrenopause is the decline in secretion and levels of adrenal androgens such as dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) from the zona reticularis of the adrenal glands with age. Levels of adrenal

neg: 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

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: Neurobiological effects of physical exercise induces the release of cortisol from the adrenal gland by activating the hypothalamic–pituitary–adrenal axis (HPA axis). Short-term increases in cortisol levels are associated with adaptive cognitive improvements, such as enhanced inhibitory control; however, excessively high exposure or prolonged exposure to high levels of cortisol causes impairments in cognitive control and has neurotoxic effects in the human brain. For example, chronic psychological stress decreases expression which has detrimental effects on hippocampal volume and can lead to depression. As a physical stressor, aerobic exercise stimulates cortisol secretion in an intensity-dependent manner; however, it does not result in long-term increases in cortisol production

neg: Sleep deprivation deprivation resulted in reduced cortisol secretion the next day, driven by increased subsequent slow-wave sleep. Sleep deprivation was found to enhance activity on the hypothalamic-pituitary-adrenal axis (which controls reactions to stress and regulates body functions such as digestion, the immune system, mood, sex, or energy usage) while suppressing growth hormones. The results supported previous studies, which observed adrenal insufficiency in idiopathic hypersomnia. A study conducted in 2005 showed that a group of rats, which were deprived of REM sleep for five days, experienced no significant changes in their ability to heal wounds, compared to a group of rats not deprived

neg: 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

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: Delta wave during sleep. Delta waves have been shown to be mediated in part by T-type calcium channels. During delta wave sleep, neurons are globally inhibited by gamma-aminobutyric acid (GABA). Delta activity stimulates the release of several hormones, including growth hormone releasing hormone GHRH and prolactin (PRL). GHRH is released from the hypothalamus, which in turn stimulates release of growth hormone (GH) from the pituitary. The secretion of (PRL), which is closely related to (GH), is also regulated by the pituitary. The release of thyroid stimulating hormone (TSH), is decreased in response to delta-wave signaling. Infants have been shown to spend a

neg: Graves' disease the thyrotropin receptor (TSH receptor) which stimulates the secretion of thyroxine (T4) and triiodothyronine (T3). Thyroxine receptors in the pituitary gland are activated by the surplus hormone, suppressing additional release of TSH in a negative feedback loop. The result is very high levels of circulating thyroid hormones and a low TSH level. Graves' disease is an autoimmune disorder, in which the body produces antibodies to the receptor for thyroid-stimulating hormone. (Antibodies to thyroglobulin and to the thyroid hormones T3 and T4 may also be produced.) These antibodies cause hyperthyroidism because they bind to the TSHr and chronically stimulate it. The

neg: Kilig kilig is usually felt in the first phase of romance, particularly during courtship or honeymoon phase in a relationship. In scientific terms, according to neuropsychologist Dr. Danilo Tuazon, hormones play a role when someone feels kilig. Those hormones that stimulate emotions include testosterone produced by the Leydig cells, adrenaline and norepinephrine, both produced by the adrenal medulla. Testosterone is for motivation while adrenaline is for the increase on one's heart rate and norepinephrine is for the regulation of emotions. Sociologist Bro. Clifford Sorita, defines kilig as an initial attraction; either having a crush or infatuating over someone. Sorita insists that

neg: Adrenal tumor Adrenal tumor An adrenal tumor or adrenal mass is any benign or malignant neoplasms of the adrenal gland, several of which are notable for their tendency to overproduce endocrine hormones. Adrenal cancer is the presence of malignant adrenal tumors, and includes neuroblastoma, adrenocortical carcinoma and some adrenal pheochromocytomas. Most adrenal pheochromocytomas and all adrenocortical adenomas are benign tumors, which do not metastasize or invade nearby tissues, but may cause significant health problems by unbalancing hormones. The adrenal cortex is composed of three distinct layers of endocrine cells which produce critical steroid hormones. These include the glucocorticoids which are critical for

neg: 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

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: Stress (biology) nucleus, release vasopressin and corticotropin releasing hormone, which travel through the hypophysial portal vessel where they travel to and bind to the corticotropin-releasing hormone receptor on the anterior pituitary gland. Multiple CRH peptides have been identified, and receptors have been identified on multiple areas of the brain, including the amygdala. CRH is the main regulatory molecule of the release of ACTH. The secretion of ACTH into systemic circulation allows it to bind to and activate Melanocortin receptor, where it stimulates the release of steroid hormones. Steroid hormones bind to glucocorticoid receptors in the brain, providing negative feedback by reducing ACTH

neg: Endocrine gland and inhibits glucose uptake and metabolism. Secretion is regulated by growth hormone releasing hormone (GHRH) and growth hormone inhibiting hormone (GHIH), or somatostatin. Hypersecretion causes gigantism in children and acromegaly in adults; hyposecretion in children causes pituitary dwarfism. Thyroid-stimulating hormone (TSH) promotes normal development and activity of the thyroid gland. Thyrotropin-releasing hormone (TRH) stimulates its release; negative feedback of thyroid hormone inhibits it. Adrenocorticotropic hormone (ACTH) stimulates the adrenal cortex to release corticosteroids. ACTH release is triggered by corticotropin-releasing hormone (CRH) and inhibited by rising glucocorticoid levels. The gonadotropins—follicle-stimulating hormone (FSH) and luteinizing hormone (LH) regulate the functions of the

neg: Cortisol Cortisol Cortisol is a steroid hormone, in the glucocorticoid class of hormones. When used as a medication, it is known as hydrocortisone. It is produced in humans by the zona fasciculata of the adrenal cortex within the adrenal gland. It is released in response to stress and low blood-glucose concentration. It functions to increase blood sugar through gluconeogenesis, to suppress the immune system, and to aid in the metabolism of fat, protein, and carbohydrates. It also decreases bone formation. In the early fasting state, cortisol stimulates gluconeogenesis (the formation of glucose), and activates antistress and anti-inflammatory pathways. Cortisol also plays

neg: Stress (biology) to stressors is particularly high. Chronic stress is seen to affect the parts of the brain where memories are processed through and stored. When people feel stressed, stress hormones get over-secreted, which affects the brain. This secretion is made up of glucocorticoids, including cortisol, which are steroid hormones that the adrenal gland releases, although this can increase storage of flashbulb memories it decreases long-term potentiation (LTP). The hippocampus is important in the brain for storing certain kinds of memories and damage to the hippocampus can cause trouble in storing new memories but old memories, memories stored before the damage, are

neg: Nerve growth factor as beta-NGF in 2012. Recent studies found that the concentration of NGF in the blood plasma is significantly higher in individuals who have been in a romantic relationship with another person for less than 12 months [227 (14) pg/ml], than those who are either not in a romantic relationship [149 (12) pg/ml] or have been in one for more than 12 months [123 (10) pg/ml]. NGF can indirectly stimulate the expression of adrenocorticotrophic hormone (ACTH) in the hypothalamic-pituitary-adrenal axis (HPA) by increasing vasopressin secretion. ACTH binds to the MC receptor in the zona fasciculata of the adrenal cortex, and stimulates

neg: Mammary gland further alveologenesis, milk protein production, and regulates osmotic balance and tight junction function. Laminin and collagen in myoepithelial basement membrane interacting with beta-1 integrin on epithelial surface again, is essential in this process. Their binding ensures correct placement of prolactin receptors on the basal lateral side of alveoli cells and directional secretion of milk into lactiferous ducts. Suckling of the baby causes release of the hormone oxytocin, which stimulates contraction of the myoepithelial cells. In this combined control from ECM and systemic hormones, milk secretion can be reciprocally amplified so as to provide enough nutrition for the baby. During weaning,

neg: Puberty into nearby cells called granulosa cells. Smaller increases of FSH induce an increase in the aromatase activity of these granulosa cells, which converts most of the testosterone to estradiol for secretion into the circulation. The remaining testosterone, together with adrenal androgens is responsible for the typical androgenic changes of female puberty: pubic hair, other androgenic hair as outlined above, body odor, acne. The bioactivity of testosterone is to a large degree limited by SHBG which in turn is mainly controlled by estradiol and prolactin levels (estradiol stimulates, prolactin decreases SHBG synthesis). Rising levels of estradiol produce the characteristic estrogenic body

neg: Nicotine dependence of the development of new nicotinic acetylcholine receptors in the brain. After several months of nicotine abstinence, the number of receptors go back to normal. Nicotine also stimulates nicotinic acetylcholine receptors in the adrenal medulla, resulting in increased levels of adrenaline and beta-endorphin. Its physiological effects stem from the stimulation of nicotinic acetylcholine receptors, which are located throughout the central and peripheral nervous systems. Chronic nicotinic acetylcholine receptor activation from repeated nicotine exposure can induce strong effects on the brain, including changes in the brain's physiology, that result from the stimulation of regions of the brain associated with reward, pleasure,

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: 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

neg: Crustacean cardioactive peptide "Periplaneta americana" by upregulating digestive hormones after the insect has fed on nutritional matter. In the crab "Cancer borealis" CCAP controls passage of food through the forgut by modulating the stomatogastric ganglion's pyloric rhythm. This suggests CCAP is involved primarily in movement of food along the gut, facilitating digestion by secretion of digestive hormones and increasing flow of blood. The effects of CCAP on the reproductive organs of females of the species "L. migratoria" have also been studied. The peptide stimulates the contraction of the oviducts and spermatheca. There is no CCAP or CCAP-like immunoreactivity shown in the oviduct or

neg: 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

neg: Italian crested newt Triturus newts plays a large role in the determination of species interactions in a natural wetland environment. Due to the larger body size of "T. carnifex", positive interactions with other smaller newt species is limited and allows for more resources and environment for "T. carnifex". During times of stress, adrenaline, noradrenaline, and dopamine are excreted from chromaffin cells located on the ventral surface of the adrenal glands. Generally these hormones are secreted from two types of chromaffin cells, but in "T. carnifex" they are only secreted from one type of chromaffin cell. The secretion of these hormones in "T. carnifex"

neg: Xenoestrogen on both wildlife and humans. The onset of puberty is characterized by increased levels of hypothalamic gonadotropin releasing hormone (GnRH). GnRH triggers the secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the anterior pituitary gland, which in turn causes the ovaries to respond and secrete estradiol. Increases in gonadal estrogen promote breast development, female fat distribution and skeletal growth. Adrenal androgen and gonadal androgen result in pubic and axillary hair. Peripheral precocious puberty caused by exogenous estrogens is evaluated by assessing decreased levels of gonadotrophins. Hormones or substances with hormone disrupting capability may interfere with pubertal development by

neg: Paraganglioma contain neurosecretory granules, only in 1–3% of cases is secretion of hormones such as catecholamines abundant enough to be clinically significant; in that case manifestations often resemble those of pheochromocytomas (intra-medullary paraganglioma). About 75% of paragangliomas are sporadic; the remaining 25% are hereditary (and have an increased likelihood of being multiple and of developing at an earlier age). Mutations of the genes for the succinate dehydrogenase, SDHD (previously known as PGL1), SDHA, SDHC (previously PGL3) and SDHB have been identified as causing familial head and neck paragangliomas. Mutations of SDHB play an important role in familial adrenal pheochromocytoma and extra-adrenal

neg: Nephron also occurs in the tubules and is active. Substances reabsorbed include: water, sodium, chloride, glucose, amino acids, lactate, magnesium, calcium, phosphate, uric acid, and bicarbonate. Substances secreted include urea, creatinine, potassium, hydrogen, and uric acid. Some of the hormones which signal the tubules to alter the reabsorption or secretion rate, and thereby maintain homeostasis, include (along with the substance affected) antidiuretic hormone (water), aldosterone (sodium, potassium), parathyroid hormone (calcium, phosphate), atrial natriuretic peptide (sodium) and brain natriuretic peptide (sodium). A countercurrent system in the renal medulla provides the mechanism for generating a hypertonic interstitium, which allows the recovery of solute-free

neg: Adolescent sexuality age 25. Partially, because of this, young adolescents are generally less equipped than adults to make sound decisions and anticipate consequences of sexual behavior, although brain imaging and behavioral correlation studies in teens have been criticized for not being causative thus possibly reaffirming cultural biases. Adolescent sexuality begins at puberty. The sexual maturation process produces sexual interest and stimulates thought processes. Subsequent sexual behavior starts with the secretion of hormones from the hypothalamus and anterior pituitary gland. These hormones target the sexual organs and begin their maturation. Increasing levels of androgen and estrogen have an effect on the thought processes

neg: Immunocontraception female mammals by the same two hormones: follicle-stimulating hormone (FSH) and luteinizing hormone (LH). The production of these in turn is induced by a single releasing hormone, gonadotropin-releasing hormone (GnRH), which has been the focus of most of the research into immunocontraception against gamete production. GnRH is secreted by the hypothalamus in pulses and travels to the anterior pituitary gland through a portal venous system. There it stimulates the production of FSH and LH. FSH and LH travel through the general circulatory system and stimulate the functioning of the gonads, including the production of gametes and the secretion of sex

neg: Phosphodiesterase 2 in various tissues, for example: adrenal medulla, brain, heart, platelet, macrophages and endothelial cells. The enzyme is thought to be involved in regulating many different intracellular processes, such as: (See review articles ) Several enzyme functions have been reported for the PDE2. It has been shown that PDE2 lowers cAMP through increased cGMP caused by atrial natriuretic peptide (ANP) resulting in decreased aldosterone secretion (See review article ). It has also been suggested that PDE2 might play an important role in the regulation of elevated intracellular concentrations of cAMP and cGMP in platelets. PDE3 is an important player in platelet

neg: IGSF1 The "IGSF1" gene is also active in the brain and in the developing liver. It can also become reactivated in liver cancer (hepatocellular carcinoma). Mice lacking a functional "Igsf1" gene similarly exhibit hypothyroidism of central origin. The "IGSF1" gene is particularly active in the pituitary gland. The pituitary synthesizes and secretes thyroid-stimulating hormone (TSH). TSH, in turn, stimulates production of the thyroid hormones, thyroxine and triiodothyronine, by the thyroid gland. TSH secretion is controlled by thyrotropin-releasing hormone (TRH), which is released by neurons in the hypothalamus of the brain. In "Igsf1" deficient mice, the receptor for TRH is downregulated in

neg: Vagus nerve vagus nerve includes axons which emerge from or converge onto four nuclei of the medulla: The motor division of the vagus nerve is derived from the basal plate of the embryonic medulla oblongata, while the sensory division originates from the cranial neural crest. The vagus nerve supplies motor parasympathetic fibers to all the organs (except the adrenal glands), from the neck down to the second segment of the transverse colon. The vagus also controls a few skeletal muscles, including: This means that the vagus nerve is responsible for such varied tasks as heart rate, gastrointestinal peristalsis, sweating, and quite a

neg: Broodiness due to the secretion of the hormone prolactin by the anterior lobe of the hypophysis. Prolactin injection in hens provokes egg laying to stop within a few days, vitellum reabsorption, ovary regression (hens only have a left ovary) and finally broodiness. However, attempts to stop broodiness by the administration of several hormones have failed because this state, once evoked, requires time to revert. Prolactin injections inhibit the production of gonadotropin hormone, a hormone that stimulates ovarian follicles which is produced in the frontal lobe of hypophysis. Castrated males can go broody with baby chicks, showing that broodiness is not limited

neg: Adrenal gland response to adrenocorticotropic hormone (ACTH) from the anterior pituitary. Cortisol is not evenly released during the day – its concentrations in the blood are highest in the early morning and lowest in the evening as a result of the circadian rhythm of ACTH secretion. Cortisone is an inactive product of the action of the enzyme 11β-HSD on cortisol. The reaction catalyzed by 11β-HSD is reversible, which means that it can turn administered cortisone into cortisol, the biologically active hormone. All corticosteroid hormones share cholesterol as a common precursor. Therefore, the first step in steroidogenesis is cholesterol uptake or synthesis. Cells

neg: Renin–angiotensin system causes blood vessels to narrow, resulting in increased blood pressure. Angiotensin II also stimulates the secretion of the hormone aldosterone from the adrenal cortex. Aldosterone causes the renal tubules to increase the reabsorption of sodium and water into the blood, while at the same time causing the excretion of potassium (to maintain electrolyte balance). This increases the volume of extracellular fluid in the body, which also increases blood pressure. If the RAS is abnormally active, blood pressure will be too high. There are many drugs that interrupt different steps in this system to lower blood pressure. These drugs are one

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