query: which part of the nephron does antidiuretic hormone act upon

pos: Vasopressin Vasopressin Vasopressin, also called antidiuretic hormone (ADH), arginine vasopressin (AVP) or argipressin, is a hormone synthesized as a peptide prohormone in neurons in the hypothalamus, and is converted to AVP. It then travels down the axon of that cell, which terminates in the posterior pituitary, and is released from vesicles into the circulation in response to extracellular fluid hypertonicity (hyperosmolality). AVP has two primary functions. First, it increases the amount of solute-free water reabsorbed back into the circulation from the filtrate in the kidney tubules of the nephrons. Second, AVP constricts arterioles, which increases peripheral vascular resistance and raises arterial

pos: Homeostasis When the hypothalamus detects a hypertonic extracellular environment, it causes the secretion of an antidiuretic hormone (ADH) called vasopressin which acts on the effector organ, which in this case is the kidney. The effect of vasopressin on the kidney tubules is to reabsorb water from the distal convoluted tubules and collecting ducts, thus preventing aggravation of the water loss via the urine. The hypothalamus simultaneously stimulates the nearby thirst center causing an almost irresistible (if the hypertonicity is severe enough) urge to drink water. The cessation of urine flow prevents the hypovolemia and hypertonicity from getting worse; the drinking of

neg: Urinary system is reabsorbed as it passes through the nephron and the remaining 1% becomes urine. The urinary system is regulated by the endocrine system by hormones such as antidiuretic hormone, aldosterone, and parathyroid hormone. The urinary system is under influence of the circulatory system, nervous system, and endocrine system. Aldosterone plays a central role in regulating blood pressure through its effects on the kidney. It acts on the distal tubules and collecting ducts of the nephron and increases reabsorption of sodium from the glomerular filtrate. Reabsorption of sodium results in retention of water, which increases blood pressure and blood volume. Antidiuretic

neg: Nephron of the urinary and reproductive organs than the rest of the nephron, the collecting duct is sometimes not considered a part of the nephron. Instead of originating from the metanephrogenic blastema, the collecting duct originates from the ureteric bud. Though the collecting duct is normally impermeable to water, it becomes permeable in the presence of antidiuretic hormone (ADH). ADH affects the function of aquaporins, resulting in the reabsorption of water molecules as it passes through the collecting duct. Aquaporins are membrane proteins that selectively conduct water molecules while preventing the passage of ions and other solutes. As much as three-quarters

neg: Common ostrich increase in haematocrit, resulting in a hypovolemic state. Two antidiuretic hormones, Arginine vasotocin (AVT) and angiotensin (AII) are increased in blood plasma as a response to hyperosmolality and hypovolemia. AVT triggers antidiuretic hormone (ADH) which targets the nephrons of the kidney. ADH causes a reabsorption of water from the lumen of the nephron to the extracellular fluid osmotically. These extracellular fluids then drain into blood vessels, causing a rehydrating effect. This drainage prevents loss of water by both lowering volume and increasing concentration of the urine. Angiotensin, on the other hand, causes vasoconstriction on the systemic arterioles, and acts as

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: Renal urea handling ions in the blood plasma. About 40% of the urea filtered is normally found in the final urine, since there is more reabsorption than secretion along the nephron. It is regulated by antidiuretic hormone, which controls the amount reabsorbed in the collecting duct system and secreted into the loop of Henle. Renal urea handling Renal urea handling is the part of renal physiology that deals with the reabsorption and secretion of urea. Movement of large amounts of urea across cell membranes is made possible by urea transporter proteins. Urea allows the kidneys to create hyperosmotic urine (urine that has more

neg: Nephrogenic diabetes insipidus content does not have an elevated glucose concentration, as opposed to diabetes mellitus. The two diseases were named (in ancient times) for the fact that one is excessive urination in which the urine tastes sweet ("diabetes mellitus") whereas the other is excessive urination in which the urine tastes unremarkable ("diabetes insipidus"). Although they shared a name, diabetes mellitus and diabetes insipidus are two separate conditions. Both cause excessive urination (hence the similarity in name), but whereas diabetes insipidus is a problem with the production of antidiuretic hormone (central diabetes insipidus) or the kidneys' response to antidiuretic hormone (nephrogenic diabetes insipidus),

neg: Syndrome of inappropriate antidiuretic hormone secretion Because not all people with this syndrome have elevated levels of vasopressin, the term "syndrome of inappropriate antidiuresis" (SIAD) has been proposed as a more accurate description of this condition. Syndrome of inappropriate antidiuretic hormone secretion Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is characterized by excessive unsuppressible release of antidiuretic hormone (ADH) either from the posterior pituitary gland, or an abnormal non-pituitary source. Unsuppressed ADH causes an unrelenting increase in solute-free water being returned by the tubules of the kidney to the venous circulation. The causes of SIADH are grouped into six categories: 1) central nervous system diseases that

neg: Syndrome of inappropriate antidiuretic hormone secretion Syndrome of inappropriate antidiuretic hormone secretion Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is characterized by excessive unsuppressible release of antidiuretic hormone (ADH) either from the posterior pituitary gland, or an abnormal non-pituitary source. Unsuppressed ADH causes an unrelenting increase in solute-free water being returned by the tubules of the kidney to the venous circulation. The causes of SIADH are grouped into six categories: 1) central nervous system diseases that directly stimulate the hypothalamus, the site of control of ADH secretion; 2) various cancers that synthesize and secrete ectopic ADH; 3) various lung diseases; 4) numerous drugs that chemically stimulate

neg: Antidiuretic antidiuretic hormone class includes vasopressin (ADH), argipressin, desmopressin, lypressin, ornipressin, oxytocin, and terlipressin. Miscellaneous others include chlorpropamide and carbamazepine. Antidiuretic An antidiuretic is a substance that helps to control fluid balance in an animal's body by reducing urination, opposing diuresis. Its effects are opposite that of a diuretic. The major endogenous antidiuretics are antidiuretic hormone (ADH; also called vasopressin) and oxytocin. Both of those are also used exogenously as medications in people whose bodies need extra help with fluid balance via suppression of diuresis. In addition, there are various other antidiuretic drugs, some molecularly close to ADH or oxytocin and

neg: Insect diuretic hormones neurohaemal sites, such as the corpora cardiaca in the brain. Before a factor can be attributed with the role of hormone, it needs to meet certain criteria. While there is evidence that some diuretic and antidiuretic factors are indeed circulating neurohormones, this has not been demonstrated for all factors investigated so far. It has been known for many years that insects possess diuretic and antidiuretic factors, but it has only been comparatively recently that technological advances have allowed for them to be characterised. Antidiuretic factors are less well studied than diuretic factors. They act either on the Malpighian tubules to

neg: Diuretic Diuretic A diuretic is any substance that promotes diuresis, the increased production of urine. This includes forced diuresis. There are several categories of diuretics. All diuretics increase the excretion of water from bodies, although each class does so in a distinct way. Alternatively, an antidiuretic, such as vasopressin (antidiuretic hormone), is an agent or drug which reduces the excretion of water in urine. In medicine, diuretics are used to treat heart failure, liver cirrhosis, hypertension, influenza, water poisoning, and certain kidney diseases. Some diuretics, such as acetazolamide, help to make the urine more alkaline and are helpful in increasing excretion

neg: Demeclocycline for the gastrointestinal tract. Demeclocycline should not be taken with food (particularly milk and other dairy products) or antacids. As with related tetracycline antibiotics, demeclocycline acts by binding to the 30S ribosomal subunit to inhibit binding of aminoacyl tRNA which impairs protein synthesis by bacteria. It is bacteriostatic (it impairs bacterial growth, but does not kill bacteria directly). Demeclocycline inhibits the renal action of antidiuretic hormone by interfering with the intracellular second messenger cascade (specifically, inhibiting adenylyl cyclase activation) after the hormone binds to vasopressin V receptors in the kidney. Exactly how demeclocycline does this has yet to be elucidated,

neg: Desmopressin is, it is an antidiuretic. It works at the level of the renal collecting duct by binding to V2 receptors, which signal for the translocation of aquaporin channels via cytosolic vesicles to the apical membrane of the collecting duct. The presence of these aquaporin channels in the distal nephron causes increasing water reabsorption from the urine, which becomes passively re-distributed from the nephron to systemic circulation by way of basolateral membrane channels. Desmopressin also stimulates release of von Willebrand factor from endothelial cells by acting on the V2 receptor. Desmopressin is degraded more slowly than recombinant vasopressin, and requires less

neg: Enuresis alarms in the brain that signal a full or emptying bladder. This form of incontinence will fade away as the bladder grows and the natural alarms become operational. Normally, the body produces a hormone that can slow the making of urine. This hormone is called antidiuretic hormone, or ADH. The body normally produces more ADH during sleep so that the need to urinate is lower. If the body does not produce enough ADH at night, the making of urine may not be slowed down, leading to bladder overfilling. If a child does not sense the bladder filling and awaken to

neg: Short-term effects of alcohol consumption and movement. This is caused by increased metabolism in areas of the brain associated with movement, such as the nigrostriatal pathway. This causes reward systems in the brain to become more active, which may induce certain individuals to behave in an uncharacteristically loud and cheerful manner. Alcohol has been known to mitigate the production of antidiuretic hormone, which is a hormone that acts on the kidney to favor water reabsorption in the kidneys during filtration. This occurs because alcohol confuses osmoreceptors in the hypothalamus, which relay osmotic pressure information to the posterior pituitary, the site of antidiuretic hormone release. Alcohol

neg: Antidiuretic Antidiuretic An antidiuretic is a substance that helps to control fluid balance in an animal's body by reducing urination, opposing diuresis. Its effects are opposite that of a diuretic. The major endogenous antidiuretics are antidiuretic hormone (ADH; also called vasopressin) and oxytocin. Both of those are also used exogenously as medications in people whose bodies need extra help with fluid balance via suppression of diuresis. In addition, there are various other antidiuretic drugs, some molecularly close to ADH or oxytocin and others not. Antidiuretics reduce urine volume, particularly in diabetes insipidus (DI), which is one of their main indications. The

neg: Syndrome of inappropriate antidiuretic hormone secretion differential, other causes should be considered as well. Cerebral salt wasting syndrome (CSWS) also presents with hyponatremia, there are signs of dehydration for which reason the management is diametrically opposed to SIADH. Importantly CSWS can be associated with subarachnoid hemorrhage (SAH) which may require fluid supplementation rather than restriction to prevent brain damage. Most cases of hyponatremia in children are caused by appropriate secretion of antidiuretic hormone rather than SIADH or another cause. How to manage SIADH depends on whether symptoms are present, the severity of the hyponatremia, and the duration. Management of SIADH includes: Raising the serum sodium concentration

neg: Fluid balance areas project to the supraoptic nucleus and paraventricular nucleus, which contain neurons that secrete the antidiuretic hormone, vasopressin, from their nerve endings in the posterior pituitary. Thus, there will be an increase in the secretion of antidiuretic hormone, causing fluid to be retained by the kidneys and urine output to be reduced. A fluid-insufficiency causes a decreased perfusion of the juxtaglomerular apparatus in the kidneys. This activates the renin–angiotensin system. Among other actions, it causes renal tubules (i.e. the distal convoluted tubules and the cortical collecting ducts) to reabsorb more sodium and water from the urine. Potassium is secreted into

neg: Hypopituitarism gland is located at the base of the brain, and intimately connected with the hypothalamus. It consists of two lobes: the posterior pituitary, which consists of nervous tissue branching out of the hypothalamus, and the anterior pituitary, which consists of hormone-producing epithelium. The posterior pituitary secretes antidiuretic hormone, which regulates osmolarity of the blood, and oxytocin, which causes contractions of the uterus in childbirth and participates in breastfeeding. The pituitary develops in the third week of embryogenesis from interactions between the diencephalon part of the brain and the nasal cavity. The brain cells secrete FGF-8, Wnt5a and BMP-4, and the

neg: Lithium (medication) the likelihood of developing depression. People taking lithium thus should routinely be assessed for hypothyroidism and treated with synthetic thyroxine if necessary. Because lithium competes with the receptors for the antidiuretic hormone in the kidney, it increases water output into the urine, a condition called nephrogenic diabetes insipidus. Clearance of lithium by the kidneys is usually successful with certain diuretic medications, including amiloride and triamterene. It increases the appetite and thirst ("polydypsia") and reduces the activity of thyroid hormone (hypothyroidism). The latter can be corrected by treatment with thyroxine and does not require the lithium dose to be adjusted. Lithium

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: Aldosterone Aldosterone Aldosterone, the main mineralocorticoid hormone, is a steroid hormone produced by the zona glomerulosa of the adrenal cortex in the adrenal gland. It is essential for sodium conservation in the kidney, salivary glands, sweat glands and colon. It plays a central role in the homeostatic regulation of blood pressure, plasma sodium (Na), and potassium (K) levels. It does so primarily by acting on the mineralocorticoid receptors in the distal tubules and collecting ducts of the nephron. It influences the reabsorption of sodium and excretion of potassium (from and into the tubular fluids, respectively) of the kidney, thereby indirectly influencing

neg: Syndrome of inappropriate antidiuretic hormone secretion ADH acts in the distal portion of the renal tubule (Distal Convoluted Tubule) as well as on the collecting duct and causes the retention of water, but "not" solute. Hence, ADH activity effectively dilutes the blood (decreasing the concentrations of solutes such as sodium), causing hyponatremia; this is compounded by the fact that the body responds to water retention by decreasing aldosterone, thus allowing even more sodium wasting. For this reason, a high urinary sodium excretion will be seen. The abnormalities underlying type D syndrome of inappropriate antidiuretic hormone hypersecretion concern individuals where vasopressin release and response are normal but

neg: Urine specific gravity the excreted molecules determines the urine's specific gravity. In adult humans, normal specific gravity values range from 1.010 to 1.030. Adults generally have a specific gravity in the range of 1.010 to 1.030 Increases in specific gravity (hypersthenuria, i.e. increased concentration of solutes in the urine) may be associated with dehydration, diarrhea, emesis, excessive sweating, urinary tract/bladder infection, glucosuria, renal artery stenosis, hepatorenal syndrome, decreased blood flow to the kidney (especially as a result of heart failure), and excess of antidiuretic hormone caused by Syndrome of inappropriate antidiuretic hormone. A specific gravity greater than 1.035 is consistent with frank dehydration.

neg: Syndrome of inappropriate antidiuretic hormone secretion of hyperglycemia (diabetes mellitus), hypertriglyceridemia, or hyperproteinia (myeloma). There are nine supplemental features: 1) a low BUN; 2) a low uric acid; 3) a normal creatinine; 4) failure to correct hyponatremia with IV normal saline; 5) successful correction of hyponatremia with fluid restriction; 6) a fractional sodium excretion >1%; 7) a fractional urea excretion >55%; 8) an abnormal water load test; and 9) an elevated plasma AVP. Antidiuretic hormone (ADH) is released from the posterior pituitary for a number of physiologic reasons. The majority of people with hyponatremia, other than those with excessive water intake (polydipsia) or renal salt wasting,

neg: Pituitary apoplexy who could be treated conservatively. After an episode of pituitary apoplexy, 80% of people develop hypopituitarism and require some form of hormone replacement therapy. The most common problem is growth hormone deficiency, which is often left untreated but may cause decreased muscle mass and strength, obesity and fatigue. 60–80% require hydrocortisone replacement (either permanently or when unwell), 50–60% need thyroid hormone replacement, and 60–80% of men require testosterone supplements. Finally, 10–25% develop diabetes insipidus, the inability to retain fluid in the kidneys due to a lack of the pituitary antidiuretic hormone. This may be treated with the drug desmopressin, which

neg: Urinary system hormone (ADH), is a neurohypophysial hormone found in most mammals. Its two primary functions are to retain water in the body and vasoconstriction. Vasopressin regulates the body's retention of water by increasing water reabsorption in the collecting ducts of the kidney nephron. Vasopressin increases water permeability of the kidney's collecting duct and distal convoluted tubule by inducing translocation of aquaporin-CD water channels in the kidney nephron collecting duct plasma membrane. Urination is the ejection of urine from the urinary bladder through the urethra to the outside of the body. In healthy humans (and many other animals), the process of urination

neg: Diuresis within the body to conserve heat. The body detects an increase in the blood pressure and inhibits the release of vasopressin (also known as antidiuretic hormone (ADH)), causing an increase in the production of urine. The "pressure" component is caused by the hydrostatic pressure of the water directly increasing blood pressure. Its significance is indicated by the fact that the temperature of the water does not substantially affect the rate of diuresis. Partial immersion of only the limbs does not cause increased urination. Thus, the hand in warm water trick (immersing the hand of a sleeping person in water to

neg: Calcitriol calcium than it loses by hormonal stimulation of osteoclasts. Only when there are conditions, such as dietary calcium deficiency or defects in intestinal transport, which result in a reduction of serum calcium does an overall loss of calcium from bone occur. Calcitriol also inhibits the release of calcitonin, a hormone which reduces blood calcium primarily by inhibiting calcium release from bone. (The effect of calcitonin on renal excretion is disputed.) Calcitriol is produced in the cells of the proximal tubule of the nephron in the kidneys by the action of 25-hydroxyvitamin D 1-alpha-hydroxylase, a mitochondrial oxygenase and an enzyme which

neg: Von Willebrand disease the secretion of luteinizing hormone and follicle-stimulating hormone from the pituitary, leading to stabilization of the endometrial surface of the uterus. Desmopressin is a synthetic analog of the natural antidiuretic hormone vasopressin. Its overuse can lead to water retention and dilutional hyponatremia with consequent convulsion. For patients with vWD scheduled for surgery and cases of vWD disease complicated by clinically significant hemorrhage, human-derived medium purity factor VIII concentrates, which also contain von Willebrand factors, are available for prophylaxis and treatment. Humate P, Alphanate, Wilate and Koate HP are commercially available for prophylaxis and treatment of vWD. Monoclonally purified factor VIII

neg: Pituitary apoplexy blood pressure (particularly on standing), low blood sugars (which can lead to coma) and abdominal pain; the low blood pressure can be life-threatening and requires immediate medical attention. Hyponatremia, an unusually low level of sodium in the blood that may cause confusion and seizures, is found in 40% of cases. This may be caused by low cortisol levels or by inappropriate release of antidiuretic hormone (ADH) from the posterior pituitary. Several other hormonal deficiencies may develop in the subacute phase. 50% have a deficiency in thyroid-stimulating hormone (TSH), leading to undersecretion of thyroid hormone by the thyroid gland and characteristic

neg: Posterior pituitary bloodstream. Insufficient secretion of vasopressin underlies diabetes insipidus, a condition in which the body loses the capacity to concentrate urine. Affected individuals excrete as much as 20 liters of dilute urine per day. Oversecretion of vasopressin causes the syndrome of inappropriate antidiuretic hormone (SIADH). Posterior pituitary The posterior pituitary (or neurohypophysis) is the posterior lobe of the pituitary gland which is part of the endocrine system. The posterior pituitary is not glandular as is the anterior pituitary. Instead, it is largely a collection of axonal projections from the hypothalamus that terminate behind the anterior pituitary, and serve as a site

neg: Nocturnal enuresis to prove and more clearly treated: Two physical functions prevent bedwetting. The first is a hormone that reduces urine production at night. The second is the ability to wake up when the bladder is full. Children usually achieve nighttime dryness by developing one or both of these abilities. There appear to be some hereditary factors in how and when these develop. The first ability is a hormone cycle that reduces the body's urine production. At about sunset each day, the body releases a minute burst of antidiuretic hormone (also known as arginine vasopressin or AVP). This hormone burst reduces the

neg: Herring bodies Herring bodies Herring bodies or neurosecretory bodies are structures found in the posterior pituitary. They represent the terminal end of the axons from the hypothalamus, and hormones are temporarily stored in these locations. They are neurosecretory terminals. Antidiuretic hormone (ADH) and oxytocin are both stored in Herring bodies, but are not stored simultaneously in the same Herring body. In addition, each Herring body also contains ATP and a type of neurophysin. Neurophysins are binding proteins, of which there are two types: neurophysin I and neurophysin II, which bind to oxytocin and ADH, respectively. Neurophysin and its hormone become a complex

neg: Hypothyroidism the blood together with elevations in antidiuretic hormone, as well as acute worsening of kidney function due to a number of causes. In most causes, however, it is unclear if the relationship is causal. A diagnosis of hypothyroidism without any lumps or masses felt within the thyroid gland does not require thyroid imaging; however, if the thyroid feels abnormal, diagnostic imaging is then recommended. The presence of antibodies against thyroid peroxidase (TPO) makes it more likely that thyroid nodules are caused by autoimmune thyroiditis, but if there is any doubt, a needle biopsy may be required. If the TSH level

neg: Homeostasis to be returned to the blood from the distal convoluted tubules or collecting ducts. This is because sodium is reabsorbed in exchange for potassium and therefore causes only a modest change in the osmotic gradient between the blood and the tubular fluid. Furthermore, the epithelium of the distal convoluted tubules and collecting ducts is impermeable to water in the absence of antidiuretic hormone (ADH) in the blood. ADH is part of the control of fluid balance. Its levels in the blood vary with the osmolality of the plasma, which is measured in the hypothalamus of the brain. Aldosterone's action on

neg: Vasopressin receptor 2 antagonists that are selective for the V2 receptor include: Their main uses are in hyponatremia, such as that caused by syndrome of inappropriate antidiuretic hormone (SIADH) and heart failure, however these agents should be avoided in patients with cirrhosis. Demeclocycline and lithium carbonate act as indirect antagonists of renal vasopressin V receptors by inhibiting activation of the second messenger cascade of the receptors. Arginine vasopressin receptor 2 has been shown to interact with C1QTNF1. Vasopressin receptor 2 Vasopressin receptor 2 (V2R), or arginine vasopressin receptor 2 (officially called AVPR2), is a protein that acts as receptor for vasopressin. AVPR2 belongs

neg: Herring bodies considered a single protein and stored in the neurohypophysis. Upon stimulation by the hypothalamus, secretory granules release said hormones into the bloodstream. Fibers from supraoptic nuclei are concerned with ADH secretion; paraventricular nuclei with oxytocin. This anatomical structure was first described by Percy Theodore Herring in 1908. Herring bodies Herring bodies or neurosecretory bodies are structures found in the posterior pituitary. They represent the terminal end of the axons from the hypothalamus, and hormones are temporarily stored in these locations. They are neurosecretory terminals. Antidiuretic hormone (ADH) and oxytocin are both stored in Herring bodies, but are not stored simultaneously

neg: Brattleboro rat Brattleboro rat The Brattleboro rat is a strain of laboratory rat descended from a litter born in West Brattleboro, Vermont in 1961 without the ability to produce the hormone vasopressin, which helps control kidney function. The rats' lack of vasopressin was the result of a naturally occurring genetic mutation. The rats were being raised for laboratory use by Dr. Henry Schroeder and technician Tim Vinton, who noticed that the litter of 17 drank and urinated excessively. The researchers determined that the rats failed to produce vasopressin, an antidiuretic hormone, and they gave the rats to Dartmouth Medical School (DMS). Researchers

neg: Hypopituitarism fixed amount of blood. Eventually, this decreases the iron levels in the body and improves the function of the organs in which iron has accumulated. Most pituitary hormones can be replaced indirectly by administering the products of the effector glands: hydrocortisone (cortisol) for adrenal insufficiency, levothyroxine for hypothyroidism, testosterone for male hypogonadism, and estradiol for female hypogonadism (usually with a progestogen to inhibit unwanted effects on the uterus). Growth hormone is available in synthetic form, but needs to be administered parenterally (by injection). Antidiuretic hormone can be replaced by desmopressin (DDAVP) tablets or nose spray. Generally, the lowest dose of

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: Vasopressin and sometimes in the distribution of vasopressin-containing axons, even when closely related species are compared. Vasopressin has shown nootropic effects on pain perception and cognitive function. Vasopressin also plays a role in autism, major depressive disorder, bipolar disorder, and schizophrenia. Vasopressin Vasopressin, also called antidiuretic hormone (ADH), arginine vasopressin (AVP) or argipressin, is a hormone synthesized as a peptide prohormone in neurons in the hypothalamus, and is converted to AVP. It then travels down the axon of that cell, which terminates in the posterior pituitary, and is released from vesicles into the circulation in response to extracellular fluid hypertonicity (hyperosmolality).

neg: Hypothalamic–pituitary–adrenal axis expressed by many different types of neurons. One important target of glucocorticoids is the hypothalamus, which is a major controlling centre of the HPA axis. Vasopressin can be thought of as "water conservation hormone" and is also known as "antidiuretic hormone." It is released when the body is dehydrated and has potent water-conserving effects on the kidney. It is also a potent vasoconstrictor. Important to the function of the HPA axis are some of the feedback loops: Release of CRH from the hypothalamus is influenced by stress, physical activity, illness, by blood levels of cortisol and by the sleep/wake cycle

neg: Small-cell carcinoma small-cell carcinoma present with metastatic disease; common sites include liver, adrenals, bone, and brain. Due to its high grade neuroendocrine nature, small-cell carcinomas can produce ectopic hormones, including adrenocorticotropic hormone (ACTH) and anti-diuretic hormone (ADH). Ectopic production of large amounts of ADH leads to syndrome of inappropriate antidiuretic hormone hypersecretion (SIADH). Lambert-Eaton myasthenic syndrome (LEMS) is a well-known paraneoplastic condition linked to small-cell carcinoma. When associated with the lung, it is sometimes called "oat cell carcinoma" due to the flat cell shape and scanty cytoplasm. It is thought to originate from neuroendocrine cells (APUD cells) in the bronchus called Feyrter

neg: Collecting duct system Collecting duct system The collecting duct system of the kidney consists of a series of tubules and ducts that physically connect nephrons to a minor calyx or directly to the renal pelvis. The collecting duct system participates in electrolyte and fluid balance through reabsorption and excretion, processes regulated by the hormones aldosterone and vasopressin (antidiuretic hormone). There are several components of the collecting duct system, including the connecting tubules, cortical collecting ducts, and medullary collecting ducts. The segments of the system are as follows: With respect to the renal corpuscle, the "connecting tubule" is the most proximal part of the

neg: Diabetes insipidus Diabetes insipidus Diabetes insipidus (DI) is a condition characterized by large amounts of dilute urine and increased thirst. The amount of urine produced can be nearly 20 liters per day. Reduction of fluid has little effect on the concentration of the urine. Complications may include dehydration or seizures. There are four types of DI, each with a different set of causes. Central DI (CDI) is due to a lack of the hormone vasopressin (antidiuretic hormone). This can be due to damage to the hypothalamus or pituitary gland or genetics. Nephrogenic diabetes insipidus (NDI) occurs when the kidneys do not respond

neg: Secretin release. It has been suggested that abnormalities in such secretin release could explain the abnormalities underlying type D syndrome of inappropriate antidiuretic hormone hypersecretion (SIADH). In these individuals, vasopressin release and response are normal, although abnormal renal expression, translocation of aquaporin 2, or both are found. It has been suggested that "Secretin as a neurosecretory hormone from the posterior pituitary, therefore, could be the long-sought vasopressin independent mechanism to solve the riddle that has puzzled clinicians and physiologists for decades." Secretin and its receptor are found in discrete nuclei of the hypothalamus, including the paraventricular nucleus and the arcuate nucleus,

neg: Nocturia atrial natriuretic hormone (ANH). AVP is an antidiuretic hormone produced in the hypothalamus and stored in and released from the posterior pituitary gland. AVP increases water absorption in the collecting duct systems of kidney nephrons, subsequently decreasing urine production. It is used to regulate hydration levels in the body. ANH, on the other hand, is released by cardiac muscle cells in response to high blood volume. When activated, ANH releases water, subsequently increasing urine production. Nocturia has four major underlying causes: global polyuria, nocturnal polyuria, bladder storage disorders, or mixed cause. The first two processes are due to irregular levels

neg: Copeptin outcome in patients suffering from heart failure has been known since the nineties. Patients presenting with high levels of vasopressin have a worsened outcome. Recently, a similar interest has been demonstrated for copeptin in heart failure. Copeptin Copeptin (also known as CT-proAVP) is a 39-amino acid-long peptide derived from the C-terminus of pre-pro-hormone of arginine vasopressin, and copeptin. Arginine vasopressin (AVP), also known as the antidiuretic hormone (ADH), is involved in multiple cardiovascular and renal pathways and abnormal level of AVP are associated with various diseases. Hence measurement of AVP would useful, but not commonly carried out in clinical practice

neg: Copeptin Copeptin Copeptin (also known as CT-proAVP) is a 39-amino acid-long peptide derived from the C-terminus of pre-pro-hormone of arginine vasopressin, and copeptin. Arginine vasopressin (AVP), also known as the antidiuretic hormone (ADH), is involved in multiple cardiovascular and renal pathways and abnormal level of AVP are associated with various diseases. Hence measurement of AVP would useful, but not commonly carried out in clinical practice because of its very short half-life making it difficult to quantify. In contrast, copeptin can be immunologically tested with ease and therefore can be used as a vasopressin surrogate marker. Copeptin is a 39-amino acid-long, glycosylated

neg: Syndrome of inappropriate antidiuretic hormone secretion where abnormal renal expression and translocation of aquaporin 2, or both are found. It has been suggested that this is due to abnormalities in the secretion of secretin in the brain and that "Secretin as a neurosecretory hormone from the posterior pituitary, therefore, could be the long-sought vasopressin independent mechanism to solve the riddle that has puzzled clinicians and physiologists for decades." There are no abnormalities in total body sodium metabolism. Hyponatremia and inappropriately concentrated urine (U >100 mOsm/L) are seen Diagnosis is based on clinical and laboratory findings of low serum osmolality and low serum sodium. Urinalysis reveals a

neg: Neurohypophysial hormone the peripheral vessels. Due to the similarity of the two hormones, there is cross-reaction: oxytocin has a slight antidiuretic function, and high levels of AVP can cause uterine contractions. In common with most active peptides, both hormones are synthesised as larger protein precursors that are enzymatically converted to their mature forms. Members of this family are found in birds, fish, reptiles and amphibians (mesotocin, isotocin, valitocin, glumitocin, aspargtocin, vasotocin, seritocin, asvatocin, phasvatocin), in worms (annetocin, nematocin), octopuses (cephalotocin), "Locusta migratoria" (Migratory locust) (locupressin or neuropeptide F1/F2) and in molluscs (conopressins G and S). Neurohypophysial hormone The neurohypophysial hormones form a

neg: Desmopressin anorexia nervosa. Desmopressin ("1-deamino-8--arginine vasopressin") is a man-made form of the normal human hormone arginine vasopressin (the antidiuretic hormone, or ADH), a peptide containing nine amino acids. Compared to vasopressin, desmopressin's first amino acid has been deaminated, and the arginine at the eighth position is in the "dextro" rather than the "levo" form (see stereochemistry). Desmopressin Desmopressin, sold under the trade name DDAVP among others, is a medication used to treat diabetes insipidus, bedwetting, hemophilia A, von Willebrand disease, and high blood urea levels. In hemophilia A and von Willebrand disease, it should only be used for mild to moderate

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: Osmoregulation e.g., glasswort and cord-grass. Mesophytes are plants living in lands of temperate zone, which grow in well-watered soil. They can easily compensate the water lost by transpiration through absorbing water from the soil. To prevent excessive transpiration they have developed a waterproof external covering called cuticle. Kidneys play a very large role in human osmoregulation by regulating the amount of water reabsorbed from glomerular filtrate in kidney tubules, which is controlled by hormones such as antidiuretic hormone (ADH), aldosterone, and angiotensin II. For example, a decrease in water potential is detected by osmoreceptors in the hypothalamus, which stimulates ADH release

neg: Azotemia the juxtaglomerular baroreceptors. Renin is secreted from granules in the JG cells, and once in the blood stream, it acts as a protease to convert angiotensinogen to angiotensin I, which is converted by angiotensin converting enzyme, to angiotensin II, which, in turn, stimulates aldosterone release. Increased aldosterone levels results in salt and water absorption in the distal collecting tubule. A decrease in volume or pressure is a nonosmotic stimulus for antidiuretic hormone production in the hypothalamus, which exerts its effect in the medullary collecting duct for water reabsorption. Through unknown mechanisms, activation of the sympathetic nervous system leads to enhanced

neg: Metolazone like indapamide, act on the same target as thiazides and behave in a similar pharmacologic fashion, they are considered "thiazide-like diuretics". Therefore, they are often included in the thiazide diuretics despite not being thiazides themselves. The primary target of all thiazide diuretics, including metolazone, is the distal convoluted tubule, part of the nephron in the kidney, where they inhibit the sodium-chloride symporter. In the kidney, blood is filtered into the lumen, or open space, of the nephron tubule. Whatever remains in the tubule will travel to the bladder as urine and eventually be excreted. The cells lining the tubule modify

neg: Urea of the loop of Henle, which makes the water reabsorb. By action of the urea transporter 2, some of this reabsorbed urea eventually flows back into the thin descending limb of the tubule, through the collecting ducts, and into the excreted urine. The body uses this mechanism, which is controlled by the antidiuretic hormone, to create hyperosmotic urine—i.e., urine with a higher concentration of dissolved substances than the blood plasma. This mechanism is important to prevent the loss of water, maintain blood pressure, and maintain a suitable concentration of sodium ions in the blood plasma. The equivalent nitrogen content (in

neg: Hyponatremia a narrow range (homeostasis of body fluid osmolality); conditions can cause that feedback system to malfunction (pathophysiology); and the consequences of the malfunction of that system on the size and solute concentration of the fluid compartments. There is a hypothalamic-renal feedback system which normally maintains the concentration of the serum sodium within a narrow range. This system operates as follows: in some of the cells of the hypothalamus, there are osmoreceptors which respond to an elevated serum sodium in body fluids by signalling the posterior pituitary gland to secrete antidiuretic hormone (ADH), (also called vasopressin). ADH then enters the bloodstream

neg: Fluoride toxicity with hypernatremia and hyperosmolarity. Inorganic fluoride inhibits adenylate cyclase activity required for antidiuretic hormone effect on the distal convoluted tubule of the kidney. Fluoride also stimulates intrarenal vasodilation, leading to increased medullary blood flow, which interferes with the counter current mechanism in the kidney required for concentration of urine. Fluoride induced nephrotoxicity is dose dependent, typically requiring serum fluoride levels exceeding 50 micromoles per liter (about 1 ppm) to cause clinically significant renal dysfunction, which is likely when the dose of methoxyflurane exceeds 2.5 MAC hours. (Note: "MAC hour" is the multiple of the minimum alveolar concentration (MAC) of the

neg: Osmotherapy inhibits these channels. Vasopressin receptors activated by vasopressin are found on the basolateral membrane of the cells lining the collecting ducts of the kidneys. Aneurysmal subarachnoid hemorrhage(aSAH) results in hyponatremia which leads to water retention and antidiuretic hormone release causing increase in intracranial pressure and formation of cerebral edema. This can be prevented by administration of conivaptan, a safe FDA approved drug that treats euvolemic hyponatremia. Through the process of aquaresis, conivapten which is a vasopressin receptor antagonist improves serum sodium concentration while eliminating free water without having any negative effect on systolic blood pressure and pulse rate. Since it

neg: Cyclophosphamide the syndrome of inappropriate antidiuretic hormone secretion (SIADH) and a potentially fatal hyponatremia when compounded by intravenous fluids administered to prevent drug-induced cystitis. While SIADH has been described primarily with higher doses of cyclophosphamide, it can also occur with the lower doses used in the management of inflammatory disorders. Acrolein is toxic to the bladder epithelium and can lead to hemorrhagic cystitis, which is associated with microscopic or gross hematuria and occasionally dysuria. Risks of hemorrhagic cystitis can be minimized with adequate fluid intake, avoidance of nighttime dosage and mesna (sodium 2-mercaptoethane sulfonate), a sulfhydryl donor which binds and detoxifies

neg: Cytochalasin B It showed that cytochalasin B enhances tumor cell lysis and stasis due to activated macrophages at a concentration of 10 M. Cytochalasin B does not act on the macrophage itself, but does exert its effect predominantly on the tumor cell. A reason for this could be, that the actin filament formation, which could be important for the destruction of tumor cells by activated macrophages, is inhibited by cytochalasin B. Cytochalasin B has an effect on thyroid hormone and growth hormone secretion. Phosphatidylcholine and phosphatidylethanolamine biosynthesis is inhibited by cytochalasin B, as shown by George et al. It does so by

neg: Lithium (medication) and kidney function for abnormalities, as it interferes with the regulation of sodium and water levels in the body, and can cause dehydration. Dehydration, which is compounded by heat, can result in increasing lithium levels. The dehydration is due to lithium inhibition of the action of antidiuretic hormone, which normally enables the kidney to reabsorb water from urine. This causes an inability to concentrate urine, leading to consequent loss of body water and thirst. Lithium concentrations in whole blood, plasma, serum or urine may be measured using instrumental techniques as a guide to therapy, to confirm the diagnosis in potential

neg: Hyponatremia urine and concentrated urine. Cases in which the urine is dilute include adrenal insufficiency, hypothyroidism, and drinking too much water or too much beer. Cases in which the urine is concentrated include syndrome of inappropriate antidiuretic hormone secretion (SIADH). High volume hyponatremia can occur from heart failure, liver failure, and kidney failure. Conditions that can lead to falsely low sodium measurements include high blood protein levels such as in multiple myeloma, high blood fat levels, and high blood sugar. Treatment is based on the underlying cause. Correcting hyponatremia too quickly can lead to complications. Rapid partial correction with 3% normal

neg: Complications of traumatic brain injury of injury, blocking blood flow to the brain. Blood clots also can develop in other parts of the head. Other types of vascular complications include vasospasm, in which blood vessels constrict and restrict blood flow, and the formation of aneurysms, in which the side of a blood vessel weakens and balloons out. Fluid and hormonal imbalances can also complicate treatment. Hormonal problems can result from dysfunction of the pituitary, the thyroid, and other glands throughout the body. Two common hormonal complications of TBI are syndrome of inappropriate secretion of antidiuretic hormone and hypothyroidism. Another common problem is spasticity. In this

neg: Syndrome of inappropriate antidiuretic hormone secretion fluid (ECF) space, there is a dilution of blood solutes, causing hypoosmolality, including a low sodium concentration - hyponatremia. Then virtually simultaneously, in the intracellular space, cells swell, i.e. intracellular volume increases. Swelling of brain cells causes various neurological abnormalities which in severe or acute cases can result in convulsions, coma, and death. Potential treatments of SIADH include restriction of fluid intake, correction of an identifiable reversible underlying cause, and/or medication which promotes solute-free water excretion by the kidney. The presence of cerebral edema may necessitate intravenous isotonic or hypertonic saline administration. SIADH was originally described in 1957 in two

neg: Syndrome of inappropriate antidiuretic hormone secretion people with small-cell carcinoma of the lung. Causes of SIADH include conditions that dysregulate ADH secretion in the central nervous system, tumors that secrete ADH, drugs that increase ADH secretion, and many others. A list of common causes is below: Normally there are homeostatic processes in the body which maintain the concentration of body solutes within a narrow range, both inside and outside cells. The process occurs as follows: in some hypothalamic cells there are osmoreceptors which respond to hyperosmolality in body fluids by signalling the posterior pituitary gland to secrete ADH. This keeps serum sodium concentration - a proxy

neg: Short-term effects of alcohol consumption causes the osmoreceptors to signal that there is low osmotic pressure in the blood, which triggers an inhibition of the antidiuretic hormone. As a consequence, one's kidneys are no longer able to reabsorb as much water as they should be absorbing, therefore creating excessive volumes of urine and the subsequent overall dehydration. Acute alcohol intoxication through excessive doses in general causes short- or long-term health effects. NMDA receptors become unresponsive, slowing areas of the brain for which they are responsible. Contributing to this effect is the activity that alcohol induces in the gamma-aminobutyric acid (GABA) system. The GABA system is

neg: Vasopressin receptor 1B feedback loop in maintaining normal central nervous system fluid balance. Vasopressin receptor 1B Vasopressin V1b receptor (V1BR) also known as vasopressin 3 receptor (VPR3) or antidiuretic hormone receptor 1B is a protein that in humans is encoded by the "AVPR1B" (arginine vasopressin receptor 1B) gene. V1BR acts as a receptor for vasopressin. AVPR1B belongs to the subfamily of G-protein coupled receptors. Its activity is mediated by G proteins which stimulate a phosphatidylinositol-calcium second messenger system.It is a major contributor to homeostasis and the control of water, glucose, and salts in the blood. Arginine vasopressin has four receptors, each of which

neg: Vasopressin receptor 1B Vasopressin receptor 1B Vasopressin V1b receptor (V1BR) also known as vasopressin 3 receptor (VPR3) or antidiuretic hormone receptor 1B is a protein that in humans is encoded by the "AVPR1B" (arginine vasopressin receptor 1B) gene. V1BR acts as a receptor for vasopressin. AVPR1B belongs to the subfamily of G-protein coupled receptors. Its activity is mediated by G proteins which stimulate a phosphatidylinositol-calcium second messenger system.It is a major contributor to homeostasis and the control of water, glucose, and salts in the blood. Arginine vasopressin has four receptors, each of which are located in different tissues and have specific functions. AVPR1b

neg: Neurohypophysial hormone There, they are stored in Herring bodies and can be released into the circulation on the basis of hormonal and synaptic signals with assistance from pituicytes. Vasopressin and oxytocin are also synthesized in the parvocellular neurosecretory cells of the paraventricular nucleus of the hypothalamus, which project to the median eminence, where they are transported and secreted into the hypophyseal portal system to stimulate the anterior pituitary. Thus they can also be considered as hypophysiotropic hormones. Oxytocin mediates contraction of the smooth muscle of the uterus and mammary gland, while vasopressin has antidiuretic action on the kidney, and mediates vasoconstriction of

neg: Adipsia Adipsia Adipsia, also known as hypodipsia, is a symptom of inappropriately decreased or absent feelings of thirst. It involves an increased osmolality or concentration of solute in the urine, which stimulates secretion of antidiuretic hormone (ADH) from the hypothalamus to the kidneys. This causes the person to retain water and ultimately become unable to feel thirst. Due to its rarity, the disorder has not been the subject of many research studies. Adipsia may be seen in conditions such as diabetes insipidus and may result in hypernatremia. It can occur as the result of abnormalities in the hypothalamus, pituitary and corpus

neg: Copeptin a reliable AVP surrogate. The clinical interest in copeptin testing is closely linked to the pathophysiological pathways in which vasopressin is involved: polydipsia-polyuria syndrome, hyponatremia, syndrome of inappropriate antidiuretic hormone secretion (SIADH) as well as heart failure and acute coronary syndrome. The concentration of copeptin in the blood circulation ranges from 1 to 12 pmol/L in healthy individuals. The levels of copeptin are slightly higher in men than in women and are not influenced by age. In response to serum osmolality fluctuations, the kinetics of copeptin are comparable to those of vasopressin. For example, patients with an electrolyte disorders such

neg: Apelin also in patients with chronic liver disease. The plasma concentration of apelin is shown to increase during exercise.. Paradoxically,exogenous apelin in healthy volunteers reduced peak VO2 in an endurance test. Apelin receptor is also expressed in the neurons of brain areas involved in regulating water and food intake. Apelin injection increases water intake and apelin decreases the hypothalamic secretion of the antidiuretic hormone vasopressin. This diuretic effect of apelin in association with its hypotensive effect participates in the homeostatic regulation of body fluid. Apelin is also detected in brain areas which control appetite, but its effects on food intake are

neg: Cerebral edema (ECF) in the brain is slightly lower than that of plasma. Plasma can be diluted by several mechanisms, including excessive water intake (or hyponatremia), syndrome of inappropriate antidiuretic hormone secretion (SIADH), hemodialysis, or rapid reduction of blood glucose in hyperosmolar hyperglycemic state (HHS), formerly known as hyperosmolar non-ketotic acidosis (HONK). Plasma dilution decreases serum osmolality, resulting in a higher osmolality in the brain compared to the serum. This creates an abnormal pressure gradient and movement of water into the brain, which can cause progressive cerebral edema, resulting in a spectrum of signs and symptoms from headache and ataxia to seizures

neg: Xerocole non-xerocoles. Desert mammals also have longer loops of Henle, structures whose efficiency in concentrating urine is directly proportional to their length. The efficiency of their loops of Henle is augmented by the increased antidiuretic hormone in their blood. Desert amphibians can store more nitrogen than aquatic ones, and do so when not enough water is available to excrete the nitrogen as urea. The African reed frog can store excess nitrogen in iridophore, pigmented granules in its skin, by converting the nitrogen to guanine, which makes up the majority of the iridophores' composition. Reptiles, birds, insects, and some amphibious species excrete

neg: Ernest Basil Verney thought"". He gave the Croonian Lecture to the society in 1947 entitled ""The antidiuretic hormone and the factors which determine its release""" He died in Cambridge in 1967. He had married Ruth Conway in 1923. Ernest Basil Verney Ernest Basil Verney FRS (22 August 1894 - 19 August 1967) was a British pharmacologist. He was born in Cardiff, Wales and attended Tonbridge School and Cambridge University, where he was awarded MA and MB. He was Sheilds Reader in Pharmacology, University of Cambridge and Professor of Pharmacology at the University of London. He was elected a Fellow of the Royal College

neg: Chlorpropamide rashes, photoallergy and (in rare cases) Stevens-Johnson syndrome. Less common side effects of chlorpropamide include gastrointestinal symptoms such as nausea, vomiting, and diarrhea. It may cause facial flushing after the ingestion of alcohol. In very high doses it can increase secretion of antidiuretic hormone (ADH), which can lead to hyponatremia. It also markedly raises the serum level of alkaline phosphatase. Chlorpropamide is a white crystalline powder with no characteristic taste or smell. It exhibits polymorphism. Its acid dissociation constant p"K" is 5.0 at 20 °C. Chlorpropamide Chlorpropamide is a drug in the sulfonylurea class used to treat diabetes mellitus type

neg: Kidney maintenance of pH around a relatively stable value. The lungs contribute to acid-base homeostasis by regulating carbon dioxide (CO) concentration. The kidneys have two very important roles in maintaining the acid-base balance: to reabsorb and regenerate bicarbonate from urine, and to excrete hydrogen ions and fixed acids (anions of acids) into urine. Maintaining water and salt level of the body. Any significant rise in plasma osmolality is detected by the hypothalamus, which communicates directly with the posterior pituitary gland. An increase in osmolality causes the gland to secrete antidiuretic hormone (ADH), resulting in water reabsorption by the kidney and an

neg: Adipsia of antidiuretic hormone (ADH). ADH secretion is one of the primary mechanisms by which sodium and osmolar homeostasis are regulated, ADH is also secreted when there are small increases in serum osmolality. Thirst is triggered by increases in serum osmolality and along with increases ADH secretion. Both serum osmolality and ADH maintain normal ranges of serum osmolality. Adipsia can tend to result from lesions to hypothalamic regions involved in thirst regulation. These lesions can be congenital, acquired, trauma, or even surgery. Lesions or injuries to those hypothalamic regions cause adipsia because the lesions cause defects in the thirst regulating center

neg: Connecting tubule cortical collecting ducts. It is this "arcuate" feature which gives the tubule its alternate name. It participates in the regulation of water and electrolytes, including sodium, and chloride. The CNT is sensitive to both isoprotenerol (more so than the cortical collecting ducts) and antidiuretic hormone (less so than the cortical collecting ducts), the latter largely determining its function in water reabsorption. Connecting tubule In the kidney, the connecting tubule (CNT, or junctional tubule, or arcuate renal tubule) is a tubular segment of the renal collecting duct system that connects the distal convoluted tubule to the cortical collecting duct. Many sources

neg: Juxtamedullary nephron Juxtamedullary nephron A juxtamedullary nephron is a type of nephron, found only in birds and mammals, which has a specific location: "medullary" refers to the renal medulla, while "juxta" (Latin: near) refers to the relative position of the renal corpuscle of this nephron - "near the medulla", but still in the cortex. In other words, a "juxtamedullary nephron" is a nephron whose renal corpuscle is near the medulla, and whose proximal convoluted tubule and its associated loop of Henle occur deeper in the medulla than the other type of nephron, the cortical nephron. Juxtamedullary nephrons are responsible for the development

neg: White adipose tissue Upon release of insulin from the pancreas, white adipose cells' insulin receptors cause a dephosphorylation cascade that lead to the inactivation of hormone-sensitive lipase. It was previously thought that upon release of glucagon from the pancreas, glucagon receptors cause a phosphorylation cascade that activates hormone-sensitive lipase, causing the breakdown of the stored fat to fatty acids, which are exported into the blood and bound to albumin, and glycerol, which is exported into the blood freely. There is actually no evidence at present that glucagon has any effect on lipolysis in white adipose tissue. Glucagon is now thought to act exclusively

neg: Syndrome of inappropriate antidiuretic hormone secretion will have elevated ADH as the cause of their hyponatremia. However, not every person with hyponatremia and elevated ADH has SIADH. One approach to a diagnosis is to divide ADH release into appropriate (not SIADH) or inappropriate (SIADH). Appropriate ADH release can be a result of hypovolemia, a so-called osmotic trigger of ADH release. This may be true hypovolemia, as a result of dehydration with fluid losses replaced by free water. It can also be perceived hypovolemia, as in the conditions of congestive heart failure (CHF) and cirrhosis in which the kidneys perceive a lack of intravascular volume. The hyponatremia

neg: Diabetes in dogs or Type 1, diabetes; research finds no Type 2 diabetes in dogs. Because of this, there is no possibility the permanently damaged pancreatic beta cells could re-activate to engender a remission as may be possible with some feline diabetes cases, where the primary type of diabetes is Type 2. There is another less common form of diabetes, diabetes insipidus, which is a condition of insufficient antidiuretic hormone or resistance to it. This most common form of diabetes affects approximately 0.34% of dogs. The condition is treatable and need not shorten the animal's life span or interfere with quality of life.

neg: Syndrome of inappropriate antidiuretic hormone secretion a normal level.] Also, virtually simultaneously to these ECF events, the intracellular space (ICF) volume expands. This is because the osmolality of the ECF is (transiently) less than that of the ICF; and since water is readily permeable to cell membranes, solute-free water moves from the ECF to the ICF compartment by osmosis: "all" cells swell. Swelling of brain cells - cerebral edema - causes various neurological abnormalities which in acute and/or severe cases can result in convulsions, coma, and death. The normal function of ADH on the kidneys is to control the amount of water reabsorbed by kidney nephrons.

neg: Department of Pharmacology at University College London, 1905 – 2007 followed his predecessor in moving to the University of Edinburgh. Ernest Basil Verney (1894–1967) succeeded Clark. He held the Chair of Pharmacology from 1926 to 1934. While at UCL Verney discovered the antidiuretic hormone and also the mechanism by which structures in the brain sense minute changes in blood osmotic pressure. Both findings were of profound importance for the understanding of water and electrolyte balance. Verney was also instrumental in arranging for Otto Krayer to come to the Department, albeit for only a short period, following Krayer's exclusion from all academic positions in German universities because of his objection to

neg: Nephrogenic diabetes insipidus Nephrogenic diabetes insipidus Nephrogenic diabetes insipidus (also known as renal diabetes insipidus) is a form of diabetes insipidus primarily due to pathology of the kidney. This is in contrast to central/neurogenic diabetes insipidus, which is caused by insufficient levels of antidiuretic hormone (ADH, that is, arginine vasopressin or AVP). Nephrogenic diabetes insipidus is caused by an improper response of the kidney to ADH, leading to a decrease in the ability of the kidney to concentrate the urine by removing free water. The clinical manifestation is similar to neurogenic diabetes insipidus, presenting with excessive thirst and excretion of a large amount

neg: Nephrogenic diabetes insipidus diabetes mellitus causes polyuria via osmotic diuresis, due to the high blood sugar leaking into the urine, taking excess water along with it. Nephrogenic diabetes insipidus Nephrogenic diabetes insipidus (also known as renal diabetes insipidus) is a form of diabetes insipidus primarily due to pathology of the kidney. This is in contrast to central/neurogenic diabetes insipidus, which is caused by insufficient levels of antidiuretic hormone (ADH, that is, arginine vasopressin or AVP). Nephrogenic diabetes insipidus is caused by an improper response of the kidney to ADH, leading to a decrease in the ability of the kidney to concentrate the urine

neg: Paraneoplastic syndrome endocrine, neurological, mucocutaneous, and hematological. The most common presentation is a fever (release of endogenous pyrogens often related to lymphokines or tissue pyrogens), but the overall picture will often include several clinical cases observed which may specifically simulate more common benign conditions. The following diseases manifest by means of endocrine dysfunction: Cushing syndrome, syndrome of inappropriate antidiuretic hormone, hypercalcemia, hypoglycemia, carcinoid syndrome, and hyperaldosteronism. The following diseases manifest by means of neurological dysfunction: Lambert-Eaton myasthenic syndrome, paraneoplastic cerebellar degeneration, encephalomyelitis, limbic encephalitis, brainstem encephalitis, opsoclonus myoclonus ataxia syndrome, anti-NMDA receptor encephalitis, and polymyositis. The following diseases manifest by means of

neg: Diabetes insipidus the postpartum period. During pregnancy, women produce vasopressinase in the placenta, which breaks down antidiuretic hormone (ADH). Gestational DI is thought to occur with excessive production and/or impaired clearance of vasopressinase. Most cases of gestational DI can be treated with desmopressin (DDAVP), but not vasopressin. In rare cases, however, an abnormality in the thirst mechanism causes gestational DI, and desmopressin should not be used. Diabetes insipidus is also associated with some serious diseases of pregnancy, including pre-eclampsia, HELLP syndrome and acute fatty liver of pregnancy. These cause DI by impairing hepatic clearance of circulating vasopressinase. It is important to consider

neg: Lung cancer worse in the developing world. Signs and symptoms which may suggest lung cancer include: If the cancer grows in the airways, it may obstruct airflow, causing breathing difficulties. The obstruction can lead to accumulation of secretions behind the blockage, and predispose to pneumonia. Depending on the type of tumor, paraneoplastic phenomena—symptoms not due to the local presence of cancer—may initially attract attention to the disease. In lung cancer, these phenomena may include hypercalcemia, syndrome of inappropriate antidiuretic hormone (SIADH, abnormally concentrated urine and diluted blood), ectopic ACTH production, or Lambert–Eaton myasthenic syndrome (muscle weakness due to autoantibodies). Tumors in the

neg: Cerebral salt-wasting syndrome lesion, tumor, or hematoma. CSWS is a diagnosis of exclusion and may be difficult to distinguish from the syndrome of inappropriate antidiuretic hormone (SIADH), which develops under similar circumstances and also presents with hyponatremia. The main clinical difference is that of total fluid status of the patient: CSWS leads to a relative or overt low blood volume whereas SIADH is consistent with a normal or high blood volume (due to water reabsorption via the V2 receptor). If blood-sodium levels increase when fluids are restricted, SIADH is more likely. Additionally, urine output is classically low in SIADH and elevated in CSWS.

neg: Blood urea nitrogen high protein diet, decrease in glomerular filtration rate (GFR) (suggestive of renal failure) and in blood volume (hypovolemia), congestive heart failure, gastrointestinal hemorrhage, fever, and increased catabolism. Hypothyroidism can cause both decreased GFR and hypovolemia, but BUN-to-creatinine ratio has been found to be lowered in hypothyroidism and raised in hyperthyroidism. The main causes of a decrease in BUN are severe liver disease, anabolic state, and syndrome of inappropriate antidiuretic hormone. Another rare cause of a decreased BUN is ornithine transcarbamylase deficiency, which is a genetic disorder inherited in an X-linked recessive pattern. OTC deficiency is also accompanied by hyperammonemia and

neg: BUN-to-creatinine ratio may be excreted in sweat. The bulk of the urea, about 10 g each day, is excreted by the kidney in a process that begins with glomerular filtration. At high urine flow rates (greater than 2 ml/min), 40% of the filtered load is reabsorbed, and at flow rates lower than 2 ml/min, reabsorption may increase to 60%. Low flow, as in urinary tract obstruction, allows more time for reabsorption and is often associated with increases in antidiuretic hormone (ADH), which increases the permeability of the terminal collecting tubule to urea. During ADH-induced antidiuresis, urea secretion contributes to the intratubular concentration

neg: Juxtamedullary nephron of the osmotic gradients in the renal medulla, which are responsible for concentrating urine because they have a longer loop of Henle than cortical nephrons. Also the hairpin bend penetrates up to the inner zone of medulla. The juxtamedullary nephron comprises only 20–30% of the nephrons in the human kidney. However, it is this type of nephron which is most often depicted in illustrations of nephrons, because their greater length and verticality makes them easier to draw. Juxtamedullary nephron A juxtamedullary nephron is a type of nephron, found only in birds and mammals, which has a specific location: "medullary" refers