Disease relevance of Pitressin

• In contrast, in conditions with water retention such as severe congestive heart failure, pregnancy, and syndrome of inappropriate antidiuretic hormone secretion, both AQP2 expression levels and apical plasma membrane targetting are increased, suggesting a role for AQP2 in the development of water retention [1].
• Hyponatremia and inappropriate secretion of vasopressin (antidiuretic hormone) in patients with hypopituitarism [2].
• That disordered thirst resulting in polydipsia was more common than true diabetes insipidus is at odds with previously held views on the prevalence of ADH deficiency in this condition [3].
• X-linked nephrogenic diabetes insipidus (NDI) is a rare disorder in which the kidney is insensitive to the antidiuretic hormone, vasopressin [4].
• Inappropriate antidiuretic hormone secretion with infectious mononucleosis [5].

Psychiatry related information on Pitressin

• Previous studies have indicated that many patients with anorexia nervosa have defects in urinary concentration or dilution suggestive of abnormal secretion of the antidiuretic hormone arginine vasopressin [6].
• The subfornical organ, a circumventricular structure of the central nervous system, has efferent neural projections to sites within the brain known to be involved in drinking behavior and secretion of antidiuretic hormone [7].
• Urinary osmolality after water deprivation for 24 h and administration of antidiuretic hormone was 2,501+/-217 and 2,874+/-392 mosmol/kg H2O in intact and uninephrectomized control rats, respectively, and 929+/-130 mosmol/kg H2O in pyelonephritic rats (P less than 0.001 compared to each control group) [8].
• While its determinants are complex, one biomolecular pathway that clearly influences social behavior is the arginine-vasopressin (AVP) system [9].
• Three patients with recurrent affective disorders experienced polydipsia and the syndrome of inappropriate secretion of antidiuretic hormone in association with acute exacerbations of their affective disorders [10].

High impact information on Pitressin

• We conclude that ACTH deficiency may cause the syndrome of inappropriate secretion of antidiuretic hormone [2].
• Demeclocycline-induced phosphate diabetes in patients with inappropriate secretion of antidiuretic hormone [11].
• Inappropriate secretion of antidiuretic hormone after transsphenoidal surgery for pituitary tumors [12].
• Five of our patients presented with polyuria and polydipsia, but only two had true diabetes insipidus, whereas three had organic primary polydipsia with adequate endogenous ADH [3].
• We hypothesized that either arginine-vasopressin (AVP) or oxytocin (OT), two nine-amino-acid neuropeptides with diverse forebrain projections, could mediate the development of selective aggression and affiliation [13].

Chemical compound and disease context of Pitressin

• Hypoglycemia provoked both CRH and AVP secretions, with the CRH increment being inversely proportional to the glucose nadir [14].
• METHODS: Renal function, plasma renin activity, and plasma concentration of aldosterone, norepinephrine, antidiuretic hormone, atrial natriuretic factor, and endothelin were measured in 9 healthy subjects, 7 compensated cirrhotics, and 25 cirrhotics with ascites (10 with functional renal failure) [15].
• In summary, portal hypertension is accompanied by a significant in vitro hyporeactivity of splanchnic vessels to norepinephrine, arginine-vasopressin, and potassium chloride, and secretion of nitric oxide in this preparation seems responsible for this blunted response [16].
• Nephrogenic diabetes insipidus, which can be inherited or acquired, is characterized by an inability to concentrate urine despite normal or elevated plasma concentrations of the antidiuretic hormone arginine vasopressin [17].
• MEASUREMENTS: Blood pressure, pulse rate, body weight, serum urea, creatinine, sodium, potassium, magnesium, osmolality, plasma antidiuretic hormone, renin, aldosterone and also urinary sodium, potassium, osmolality, and cyclic adenosine monophosphate (cAMP) before and 6 to 8, 12, and 24 hours after drug administration [18].

Biological context of Pitressin

• Arginine-vasopressin (AVP) is a neurohypophysial nonapeptide with antidiuretic activity involved in the control of blood volume and plasma osmolality [19].
• Physiological levels of arginine-vasopressin suppress diuresis and produced vasoconstriction [20].
• Numerous investigators have concluded that ADH-induced water reabsorption causes large apparent increases in cell volume with concomitant cytoplasmic dilution [21].
• We conclude that prolonged exposure to high altitude may result in persistent impairment of osmoregulation, caused in part by an inappropriate arginine-vasopressin response to hyperosmolality [22].
• Body fluid homeostasis requires the release of arginine-vasopressin (AVP, an antidiuretic hormone) from the neurohypophysis [23].

Anatomical context of Pitressin

• Influence of antidiuretic hormone on release of lysosomal hydrolase at mucosal surface of epithelial cells from urinary bladder [24].
• These findings suggest that left atrial stretch receptors, which influence secretion of antidiuretic hormone when stimulated, may also play an important role in mediating thirst during hypovolemia [25].
• Syndrome of inappropriate secretion of antidiuretic hormone: association with cavernous sinus thrombosis [26].
• The neuroendocrine mechanisms for stress hyporesponsiveness are likely to include reduced synthesis and secretion of corticotropin releasing hormone (CRH) and arginine vasopressin (AVP) from the hypothalamus as a result of enhanced glucocorticoid negative feedback and/or reduced noradrenergic stimulatory input from the brain stem [27].
• Indeed, AVP-releasing neurons in the supraoptic nucleus (SON) are directly osmosensitive, and this osmosensitivity is mediated by stretch-inhibited cation channels [23].

Associations of Pitressin with other chemical compounds

• Using tritiated arginine-8-vasopressin [3H]AVP, vasopressin-specific binding sites were detected on human platelet membranes [28].
• Whereas steady state levels of OT mRNA were markedly increased throughout lactation, those of AVP mRNA were only transiently (initially) elevated, and the blood levels of these hormones were not significantly altered in lactating as compared with cycling virgin and postlactating rats [29].
• The action sites for parathyroid hormone (PTH), salmon calcitonin (SCT), and arginine-vasopressin (AVP) were investigated along the human nephron by measuring adenylate cyclase activity, using a single tubule in vitro microassay [30].
• This paper describes the inhibitory effect of prostaglandin E2 (PGE2) on antidiuretic hormone (ADH)-stimulated net Cl- absorption and spontaneous transepithelial voltage (Ve) in single medullary thick ascending limbs of Henle (TALH, thick ascending limb; mTALH, medullary segment; cTALH, cortical segment) obtained from mouse kidney [31].
• Roles of Ca2+ and Na+ on the modulation of antidiuretic hormone action on urea permeability in toad urinary bladder [32].

Gene context of Pitressin

• Cold stress for 30 min also stimulates an increase in the percentage of immunoreactive corticotropes and cells that bind CRH or arginine vasopressin (AVP) [33].
• AVP that participates in the regulation of ACTH release at the pituitary level is produced in two main groups of neurons in the hypothalamus: parvicellular cells in the paraventricular nucleus, which also produce CRF-41, and magnocellular neurons in the supraoptic and paraventricular nuclei [34].
• Moreover, Trpv1(-/-) mice showed a pronounced serum hyperosmolality under basal conditions and severely compromised AVP responses to osmotic stimulation in vivo [23].
• Arginine-vasopressin (AVP) is a hormone that is essential for both osmotic and cardiovascular homeostasis, and exerts important physiological regulation through three distinct receptors, V1a, V1b, and V2 [35].
• The functional viability of these ARC/PVN cultures was verified by their ability to synthesize and secrete CRH, AVP, and beta-END under basal and depolarizing (veratridine) conditions in vitro [36].

Analytical, diagnostic and therapeutic context of Pitressin

• Molecular cloning of the receptor for human antidiuretic hormone [37].
• The present studies were designed to, first, determine whether a urinary concentrating defect exists in potassium-depleted rabbits and, second, to use the technique of in vitro perfusion to evaluate directly the antidiuretic hormone (ADH) responsiveness of cortical collecting tubules (CCT) in this setting [38].
• The effects of maximal physiological doses of arginine-8-vasopressin ([Arg8]VP (herein designated AVP); 20 pg/min per 100 g of body weight) were studied 2 days after the cessation of treatment, when the animals had returned to DI [39].
• RNase protection and heteroduplex analyses demonstrate that, in heterozygous animals, which express both alleles of the AVP gene, the wild-type but not the mutant transcript is subject to axonal compartmentation [40].
• Exposure of ARC/PVN cocultures to the glucocorticoid dexamethasone (DEX) resulted in a dose-dependent increase of CRH secretion and an inhibition of AVP and beta-END; the CRH responses deviated strikingly from predictions based on in vivo experiments [36].

References