Disease relevance of Vasopressin

• Central release of vasopressin (VP) by the magnocellular neuroendocrine cells (MNCs) responsible for systemic VP release is believed to be important in modulating the activity of these neurons during dehydration [1].
• In addition, LPS-induced endotoxemia causes disturbances of the magnocellular vasopressinergic system with an unexpected potentiation of osmotic simulated VP secretion [2].
• The subpopulation of corticotropin-releasing hormone (CRH) neurosecretory cells that contains vasopressin (VP) is selectively activated by several types of stress (immobilization, hypoglycemia, and intracerebroventricular, i.c.v., colchicine), and is located in a catecholamine-rich area of the hypothalamic paraventricular nucleus [3].
• In contrast, the levels of corticotropin-releasing hormone (CRH) and vasopressin (VP) mRNAs in the hypothalamic paraventricular nucleus (PVN) as well as of VP mRNA in the supraoptic nucleus (SON) were unaffected by maternal undernutrition [4].
• The results suggest that AVT, normally released during hemorrhage and dehydration, would increase lymph heart output and help compensate for the hypovolemia [5].

Psychiatry related information on Vasopressin

• Water deprivation resulted in marked increases in plasma osmolarity and vasopressin (VP) levels and hypothalamic VP mRNA and immunoreactive (ir) VP in magnocellular neurons [6].
• Two experiments were performed aiming (i) to investigate the impact of sleep on the response to a combined CRH/VP administration and (ii) to specify the onset of sleep associated pituitary-adrenal suppression and its relation to specific sleep stages [7].
• The increase of ACTH and cortisol concentrations after combined VP/CRH administration was distinctly higher during wakefulness than sleep (P < 0.01) [7].

High impact information on Vasopressin

• Systemic or i.c.v. injections of VT markedly inhibit the expression of all aspects of male sexual behavior [8].
• The absence of an effect on CRH/VP-induced pituitary-adrenal responses suggests a direct action of the peptide on the central nervous system inhibiting stimulated hypothalamo-pituitary-adrenal activity at the hypothalamic level [9].
• Furthermore, somatodendritic VP release elicited by acute dehydration is blocked by PAC(6-27), suggesting that endogenous PACAP participates in this response [1].
• A potential role for PACAP in promoting efficient, but not exhaustive, systemic release of VP from MNCs during physiological challenge is discussed [1].
• We first determined whether alcohol acted within the brain to stimulate neurons in the paraventricular nucleus (PVN) of the hypothalamus, which synthesizes corticotropin-releasing factor (CRF) and vasopressin (VP) [10].

Chemical compound and disease context of Vasopressin

• NE increased TPR significantly greater (P < 0.01) in hypertension than normotension, as did PE infusion, whereas ANG II and VP increased TPR similarly before and after hypertension [11].

Biological context of Vasopressin

• These results suggest that the control of VT gene expression is different in males and females during spawning migration, although the neuroendocrine mechanism is not known [12].
• The intensities of hybridization signals for VT and IT mRNAs, as well as immunoreactivity of VT and IT, showed seasonal variations, although the profiles were different between the ordinary and precocious males [13].
• In saline-treated SHR, blood pressure rose significantly and the number of VP parvocellular cells was reduced by about 60% relative to WKY [14].
• An intravenous injection of arginine vasotocin (AVT) caused the increase in the uterine PGF concentration and induced oviposition [15].
• Tolvaptan (Otsuka) is an orally administered nonpeptide vasopressin (VP) V2 receptor antagonist that inhibits water reabsorption in the kidney by competitively blocking VP binding, resulting in water diuresis without significantly changing total electrolyte excretion [16].

Anatomical context of Vasopressin

• Central VP release from MNC somata and dendrites is stimulated by both dehydration and pituitary adenylate cyclase activating polypeptide (PACAP) [1].
• The levels of VT and IT mRNA in the forebrains were determined by quantitative Northern blot analysis using single-stranded DNA with the same mRNA sequences as the standards [12].
• The lack of increase in VP transcription after LPS and changes in VP mRNA distribution suggest that endotoxemia affect the secretory process at the levels of the neurohypophyseal axon terminal [2].
• Hypothalamic parvocellular vasopressin (VP) and corticotropin-releasing hormone (CRH) in the paraventricular nucleus (PVN) are major secretagogues of corticotropin (ACTH), and central plasticity including their alteration is closely related to hypothalamic-pituitary-adrenal (HPA) axis modulation [17].
• In addition, and despite comparable PVN VP transcript levels, the lower levels of this peptide in the median eminence also may participate in the blunted ACTH response that we observed [18].

Associations of Vasopressin with other chemical compounds

• Thirty minutes after intranasal administration of ANP (1 mg) and placebo, pituitary-adrenal activity was stimulated in 18 healthy men by two tests: 1) a standard insulin-hypoglycemia test and 2) CRH combined with vasopressin (VP), respectively [9].
• We analyzed changes in the hypothalamic levels of vasotocin (VT) and isotocin (IT) mRNA in chum salmon during spawning migration to the Ishikari river [12].
• The habituated, vehicle-injected sham control group had normal levels of plasma ACTH and corticosterone, but possessed a significantly higher proportion of VP-containing CRH axons than naive animals [3].
• The degree of activation of OT/VP neurons paralleled the magnitude of aversive response to a given treatment [19].
• The results suggest that DAG accumulation that is sustained for many hours in response to VP, Ang.II, NE, and prostaglandin F2alpha in hepatocytes is mainly due to phosphoinositide breakdown [20].

Gene context of Vasopressin

• V1b receptor mRNA levels and coupling of the receptor to phospolipase C are stimulated by glucocorticoids, effects which may contribute to the refractoriness of VP-stimulated ACTH secretion to glucocorticoid feedback [21].
• In the latter case, the rise in plasma ACTH levels, adenopituitary POMC gene expression, hypothalamic VP gene expression, and the decrease in hippocampal MR gene expression in DG and GR gene expression in CA3 and DG observed in controls are lacking in FR50 rats [4].
• Chromatography of the native plasma on a AcA 34 column revealed two peaks inhibiting the PTH and to a lesser extent the VP dependent AC [22].
• Experimental animals with VIP and VP/NP II immunoreactivity in the SCN within the island retained free-running locomotor rhythms following transection of SCN efferents [23].
• Both the POMC and the ACTH responses were completely abolished by removal of CRF and VP [10].

Analytical, diagnostic and therapeutic context of Vasopressin

• These changes reflect modifications of VT mRNA concentrations (and probably synthesis) as demonstrated by in situ hybridization and they are paralleled by similar changes in male copulatory behavior (absent in castrated male quail, fully expressed in CX+T males) [8].
• These results indicate that the HPA axis activity of parvocellular neurons is still altered at 1 week of rehydration and that VP plays a dominant role in regulating ACTH release in response to acute stress [17].
• In contrast to the above, intravenous injections of relaxin (40 micrograms/kg) elicited pressor and tachycardic responses that were not blunted by pretreatment with either intracerebroventricular or intravenous injection of the V1 receptor antagonist [24].
• The increase in VT mRNA was reflected in the plasma level of peptide; plasma VT concentration measured by highly sensitive and specific radioimmunoassay increased according to elevated environmental salinities [25].
• If AVT is actually a hormone in fishes, its primary actions may be vasopressor, and the effects of exogenous AVT on GFR and urine flow may represent a pharmacological response to elevated renal perfusion pressure [26].

References