Vasopressin inappropriate release

Causes of nonosmotic release of arginine vasopressin, commonly known as antidiuretic hormone, include hypovolemia decreased effective circulating volume as seen in patients with congestive heart failure nephrosis cirrhosis and syndrome of inappropriate antidiuretic hormone (SIADH) release. 

The most important stimulus to the release of ANP from the heart is atrial stretch via mechanosensitive ion channels. ANP release is also increased by volume expansion, changing from the standing to the supine position, and exercise. ANP release can also be increased by sympathetic stimulation via aiA-adrenoceptors, endothelins via the -receptor subtype (see below), glucocorticoids, and vasopressin. Plasma ANP concentration increases in various pathologic states, including heart failure, primary aldosteronism, chronic renal failure, and inappropriate ADH secretion syndrome. 

The autonomous, sustained production of AVP in the absence of known stimuli for its release is called SIADH. In this syndrome, plasma AVP concentrations are inappropriately increased relative to a low plasma osmolality and to a normal or increased plasma volume. SIADH may be the result of one of several factors production of vasopressin by a malignancy (such as a small cell carcinoma of the lung), the presence of acute and chronic diseases of the central nervous system, pulmonary disorders, or a side effect of certain drug therapies. In addition, as many as 10% of patients undergoing pituitary surgery have a transient SIADH approximately 8 to 9 days after surgery (when the patient is at home), which responds to water restriction (2 to 3 days) and resolves without recurrence. In SIADH, a primary excess of AVP, coupled with unrestricted fluid intake, promotes increased reabsorption of free water by the kidney. The result is a decreased urine volume and an increased urine sodium concentration and urine osmolality. As a consequence of water retention, these patients become modestly volume expanded. The increase in intravascular volume causes hemodilution accompanied by dilutional hyponatremia and a low plasma osmolality. Volume expan-... 

A variety of endocrine effects have been reported Inhibition of vasopressin release has been observed in patients with inappropriate secretion of this hormone. Hyperglycemia and glycosuria appear to be due to inhibition of insulin secretion. Osteomalacia has been attributed to altered metabolism of vitamin D and the attendant inhibition of intestinal Ca absorption. Phenytoin also increases the metabolism of vitamin K and reduces the concentration of vitamin K-dependent proteins that are important for normal metabolism in bone, perhaps explaining why the osteo-... 

Vasopressin and oxytocin or one or several precursors of them are produced in the pericarya of cells in certain nuclei of the hypothalamus and maybe also within the axons leading from these cell bodies to the neural lobe of the pituitary. The hormones or their precursors are transported in neurosecretory granules from the perikarya of the cells to the neural lobe where they are stored and from where the controlled release takes place. The appropriate (or inappropriate) stimuli for release produce nerve signals, the last pathway of which is the nerve membrane surrounding the terminal swellings of the axon. There is no information on the speed with which the neurosecretory granules move within the axons. 

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