Osmoreceptor

Logically, ADH receptor antagonists, and ADH synthesis and release inhibitors can be effective aquaretics. ADH, 8-arginine vasopressin [113-79-17, is synthesized in the hypothalamus of the brain, and is transported through the supraopticohypophyseal tract to the posterior pituitary where it is stored. Upon sensing an increase of plasma osmolaUty by brain osmoreceptors or a decrease of blood volume or blood pressure detected by the baroreceptors and volume receptors, ADH is released into the blood circulation it activates vasopressin receptors in blood vessels to raise blood pressure, and vasopressin V2 receptors of the nephrons of the kidney to retain water and electrolytes to expand the blood volume. 

The primary factor that influences ADH secretion is a change in plasma osmolarity. Osmoreceptors in the hypothalamus are located in close proximity to the ADH-producing neurosecretory cells. Stimulation of these osmoreceptors by an increase in plasma osmolarity results in stimulation of the neurosecretory cells an increase in the frequency of action potentials in these cells and the release of ADH from their axon terminals in the neurohypo-... 

Hypothalamic osmoreceptors have a threshold of 280 mOsM. Below this value, they are not stimulated and little or no ADH is secreted. Maximal ADH levels occur when plasma osmolarity is about 295 mOsM. Within this range, the regulatory system is very sensitive, with measurable increases in ADH secretion occurring in response to a 1% change in plasma osmolarity. Regulation of ADH secretion is an important mechanism by which a normal plasma osmolarity of 290 mOsM is maintained. 

Explain how each of the three types of sensory receptors within the digestive tract is stimulated chemoreceptors, osmoreceptors, and mechanoreceptors... 

The osmoreceptors of the hypothalamus monitor the osmolarity of extracellular fluid. These receptors are stimulated primarily by an increase in plasma osmolarity they then provide excitatory inputs to the thirst center and the ADH-secreting cells in the hypothalamus. The stimulation of the thirst center leads to increased fluid intake. The stimulation of the ADH-secreting cells leads to release of ADH from the neurohypophysis and, ultimately, an increase in reabsorption of water from the kidneys and a decrease in urine output. These effects increase the water content of the body and dilute the plasma back toward normal. Plasma osmolarity is the major stimulus for thirst and ADH secretion two additional stimuli include ... 

Liedtke, W., Choe, Y., Marti-Renom, M.A., Bell, A.M., Denis, C.S., Sali, A., Hudspeth, A.J., Friedman, J.M., Heller, S. Vanilloid receptor-related osmotically activated channel (VR-OAC), a candidate vertebrate osmoreceptor, Cell 2000, 103, 525-535. 

Jung J S, Bhat R V, Preston G M, Guggino W B, Baraban J M, Agre P. 1994. Molecular chracterization of an aquaporin cDNA from brain candidate osmoreceptor and regulator of water balance. Proc Natl Acad Sci USA 91 13052-13056. 

Thus, if osmoreceptors sense that osmolarity of the bloodstream is higher than normal, the secretion of vasopressin is increased. In addition, the patient experiences a thirst sensation, although a different set of osmoreceptors is in-... 

Q9 Loss of albumin through the glomerular membrane reduces the concentration of albumin in the blood. Albumin plays a major role in the maintenance of ECF volume, and when there is a deficiency additional fluid passes from plasma into the tissues to form oedema. Passage of extra fluid from the circulation into the tissues reduces blood volume, which stimulates the renin-angiotensin system and also triggers the thirst mechanism via osmoreceptors in the hypothalamus. 

Regulation of anti-diuretic hormone secretion is primarily through the plasma osmolarity. Osmolarity is sensed in the hypothalamus by neurons known as osmoreceptors, which in turn stimulate secretion from those neurons that produce anti-diuretic hormone. Secretion of antidiuretic hormone is also simulated by decreases in blood pressure and volume, conditions sensed by stretch receptors in the heart and large arteries. Changes in blood pressure and volume are not nearly as sensitive a stimulator as increased osmolarity, but are nonetheless potent in severe conditions. For example, loss of 15-20% of blood volume by haemorrhage results in a massive secretion of anti-diuretic hormone. Another potent stimulus of anti-diuretic hormone is nausea and vomiting, both of which are controlled by regions in the brain with links to the hypothalamus. 

Barker, G.R., Cochrane, G.M., Corbett, G.A., Hunt, J.N, Roberts, S.K. (1974) Actions of glucose and potassium chloride on osmoreceptors slowing gastric emptying. J. Physiol. (London) 237, 183-186. 

Apprehension and fear caused an increase in blood levels, but the induction of anesthesia was not a strong stimulus. ADH levels are often raised in the preoperative patient owing to fiuid deprivation, and intravenous fluids will frequently cause a reduction in plasma ADH activity. Skin incision in a patient under general anesthesia constitutes a stimulus which can be abolished by the additional use of a local anesthetic in the skin (M6). Traction on the root of the mesentery of the small intestine was shown to be a distinct stimulus. Osmoreceptors are involved in the control of ADH release, which is inhibited when tonicity is low and is increased as tonicity rises (H12). However, after injury when the plasma is often hypotonic for many reasons and the urine concentrated, the promotion of further antidiuresis is paradoxical and unrelated to normal mechanisms of osmolality control. Plasma volume changes and associated deprivation of intake in the immediate post injury period take precedence over tonicity control mechanisms. Thus many stimuli which in themselves are not associated with blood volume changes can evoke an ADH response. 

The stomach empties liquids faster than solids. The rate of transfer of gastric contents to the small intestine is retarded by the activity of receptors sensitive to acid, fat, osmotic pressure and amino acids in the duodenum and the small intestine and stimulated by material that has arrived from the stomach. Gastric emptying is a simple exponential or square-root function of the volume of a test meal - a pattern that holds for meals of variable viscosity. To explain the effect of a large range of substances on emptying, an osmoreceptor has been postulated which, like a red blood cell, shrinks in hypertonic solutions and swells in hypotonic solutions. 

Besides the osmoreceptor mechanism of vasopressin release, the physiological regulation of vasopressin secretion also involves a pressure-volume mechanism that is distinct from the osmotic sensor. AVP release is regulated by baro-receptors that respond to alterations in blood volume. For example, a reduction in plasma volume or arterial pressure,... 

The thirst center is regulated by many of the same factors that determine AVP release. This center has a higher set point than the osmoreceptors and responds to osmolalities above 290mOsm/kg. Responses involving AVP, thirst, and the kidney are coordinated in a complex scheme to maintain plasma osmolality in healthy individuals within a narrow range (284 to 295mOsm/kg). 

The rate of passage of food into the duodenum depends on the type of food and on the osmotic pressure it exerts in the duodenum. Food rich in fat moves most slowly, food rich in carbohydrate moves most rapidly, and food rich in protein moves at an intermediate rate. Hyperosmolality decreases gastric emptying via duodenal osmoreceptors. Some GI hormones also inhibit gastric motility and secretion. 

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