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Adipsia, also known as hypodipsia, is a symptom of inappropriately decreased or absent feelings of thirst. [1] [2] 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 ...
551 11998 Ensembl ENSG00000101200 ENSMUSG00000037727 UniProt P01185 P35455 RefSeq (mRNA) NM_000490 NM_009732 RefSeq (protein) NP_000481 NP_033862 Location (UCSC) Chr 20: 3.08 – 3.08 Mb Chr 2: 130.42 – 130.42 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Human vasopressin, also called antidiuretic hormone (ADH), arginine vasopressin (AVP) or argipressin, is a hormone synthesized ...
After synthesis, the hormone is transported in neurosecretory granules down the axon of the hypothalamic neuron to the posterior lobe of the pituitary gland, where it is stored for later release. In addition, the hypothalamus regulates the sensation of thirst in the ventromedial nucleus by sensing increases in serum osmolarity and relaying this ...
The syndrome of inappropriate antidiuretic hormone secretion (SIADH), also known as the syndrome of inappropriate antidiuresis (SIAD), [2] is characterized by a physiologically inappropriate release of antidiuretic hormone (ADH) either from the posterior pituitary gland, or an abnormal non-pituitary source. [1]
An antidiuretic is a substance that helps to control fluid balance in an animal's body by reducing urination, [1] opposing diuresis. [2] Its effects are opposite that of a diuretic . The major endogenous antidiuretics are antidiuretic hormone (ADH; also called vasopressin) and oxytocin .
Vasopressin is used to manage anti-diuretic hormone deficiency. It has off-label uses and is used in the treatment of gastrointestinal bleeding, ventricular tachycardia and ventricular defibrillation. Vasopressin is used to treat diabetes insipidus related to low levels of antidiuretic hormone. It is available as Pressyn. [6]
These receptors trigger the release of antidiuretic hormone (ADH). [22] ADH resists dehydration by increasing water absorption in the kidneys and constricting blood vessels. It acts on the V2 receptors in the cells of the collecting tubule of the nephron to increase expression of aquaporin.
In 1953, Leaf et al., demonstrated that exogenous administration of the antidiuretic hormone vasopressin resulted in hyponatremia and a natriuresis dependent on water retention and weight gain. This was not "salt wasting"; it was a physiologic response to an expanded intravascular volume.