Disease relevance of AVP

• When hypoglycemia is deeper, AVP secretion becomes predominant and may by itself stimulate ACTH release [1].
• These results show that, in fetal sheep, high concentrations of glucocorticoid near the fetal PVN prevent increases in plasma ACTH secretion seen in controls in response to hypotension and hypoxemia, and exert at least part of their effect at the level of the CRH- and AVP-producing neurons located in the PVN [2].
• With the possible exception of AVP it appears unlikely that the acute systemic hormone response to hemorrhage is determined by hormone changes in CSF [3].
• 4. We conclude that carotid denervation does not affect plasma [AVP] during hypoxia in fetal sheep [4].
• 2. During the period of fixed water intake, the EGF-treated ewes experienced mild dehydration with elevated plasma osmolality, sodium, renin and arginine vasopressin (AVP) concentrations and slightly reduced plasma atrial natriuretic peptide (ANP) concentrations [5].

Psychiatry related information on AVP

• Eighteen hr of water deprivation evoked a 7-fold increase in AVP [6].
• Little is known about adrenal regulation of AVP and CRH immediately prior to this critical period [7].
• Thus satiation was not necessary for rapid inhibition of AVP release after drinking, but satiation was necessary for this inhibition to be maintained [8].

High impact information on AVP

• Comparison of the amino acid sequence of prepro-CRF with those of the ACTH-beta-LPH precursor and the arginine vasopressin-neurophysin II precursor suggests that these precursor proteins may be evolutionarily related [9].
• NE (50 micrograms) increased mean hypophysial-portal corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) levels (1 h, 1.3- and 2.9-fold; 4 h, 2.2- and 5.7-fold) and caused acute and sustained increases in mean plasma ACTH and cortisol [10].
• When added to cultured ovine anterior pituitary cells, NPY neither increased basal ACTH release nor augmented CRF- or AVP-induced ACTH release [10].
• This study was undertaken to define the roles of corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) in the regulation of adrenocorticotropin (ACTH) release and biosynthesis in cultured ovine anterior pituitary cells and to define the intracellular mechanisms responsible for their action [11].
• A 30-min incubation with phorbol 12-myristate 13-acetate (PMA) caused a dose-related translocation of protein kinase C from the cytosol to the cell membrane; after 4 h, the increases in ACTH release and total ACTH content in response to increasing concentrations of PMA were similar to those caused by AVP [11].

Chemical compound and disease context of AVP

• 6. AVP plasma levels correlated negatively with fever magnitude following premature birth induced by dexamethasone [12].
• Each ewe was subjected to saline control infusion, nitroprusside-induced hypotension (100 micrograms/min for 10 min), insulin-induced hypoglycemia (25 U porcine insulin), CRF (1 microgram/min for 60 min), AVP (0.2 microgram/min), and a combination of CRF plus AVP [13].
• These results show that in conscious sheep rapid and major increases in plasma AVP, ACTH, and AII follow acute moderate hemorrhage [3].
• However, neither isolation nor dehydration altered the expression of mRNA for vasopressin (AVP) in either the PVN or the SON [14].
• Moderate hypoxemia (pO2 16 +/- 2 torr and 33 +/- 6 torr in fetus and neonate, respectively) induced increases in E, NE (measured by radioenzymatic assay), and AVP (measured by radioimmunoassay) in both fetus and neonate [15].

Biological context of AVP

• RIA measurements of ACTH secretion by cell populations showed that the response of corticotrophs to CRH diminished, whereas that to AVP increased during gestation and into adulthood [16].
• Furthermore, the plasma osmolality threshold for AVP secretion was significantly higher in Dehy singletons (290 +/- 2 mOsm/kg) than Control twins (285 +/- 1 mOsm/kg) and Control singletons (280 +/- 2 mOsm/kg), indicating in utero programming of an altered set point for systemic osmolality and blood pressure regulation [17].
• We examined the hypothesis that pituitary ACTH output in response to arginine vasopressin (AVP) and CRF separately and together might change during late pregnancy as a function of fetal age [18].
• 3. In the denervated fetuses no significant bradycardia, fall in femoral blood flow or increase in femoral vascular resistance was present soon after the onset of hypoxia but plasma AVP increased to similar concentrations to those observed in intact fetuses during hypoxia [4].
• 4. The amounts of AVP in perfusates from the septal region correlated negatively with changes in body temperature [12].

Anatomical context of AVP

• In five fetuses challenged with AVP (1 microgram/ml, iv bolus) plasma ACTH concentrations increased to an 8-fold peak within 10 min of the preceding baseline (55 +/- 6 to 403 +/- 241 pg/ml) [19].
• The purpose of this study was to determine whether normal morphological development occurs in pituitary corticotrophs deprived of products of the hypothalamic paraventricular nucleus (PVN), e.g. corticotropin releasing hormone and arginine vasopressin (AVP), after PVN lesions [20].
• AVP staining was strong in the internal zone of the median eminence in all groups, but was absent in the external zone of PVNX fetuses only [20].
• 3. Intracerebroventricular infusion of low-Na+ artificial cerebrospinal fluid (CSF) reduced CSF Na+ concentration, decreased plasma vasopressin (AVP) levels and caused a copious water diuresis [21].
• 3. Loci in which AVP induced antipyresis were limited to the septal region about 2-3 mm anterior to the anterior commissure [12].

Associations of AVP with chemical compounds

• We studied the effects of IIH on the secretion of CRF and AVP in HPB and on the release of ACTH and cortisol in peripheral plasma in conscious, unrestrained, castrated rams [1].
• Conscious ewes received i.m. injections of a selective AVP V2-receptor agonist (1-desamino, D-Arg8 vasopressin acetate, DDAVP) every 12 hours for days 5 to 16 [22].
• Arginine vasopressin (AVP) immunostaining of PVN of DEX and CHOL fetuses was similar; however, unlike CHOL, DEX fetuses showed no AVP immunostaining of the external zone of median eminence [2].
• Similar increases in the fetal plasma concentrations of ACTH, AVP, noradrenaline and adrenaline were observed during hypoxaemia in both groups; however, both the increments in fetal plasma concentration of cortisol in response to acute hypoxaemia and to exogenous ACTH were blunted in twins relative to singletons [23].
• Short term cultured pituitary cells from fetal (63-144 days old) and young lambs (30-120 days old) were tested for their in vitro ability to release immunoreactive ACTH and cAMP in response to stimulation by ovine (o) oCRF1-41, arginine vasopressin (AVP), epinephrine, and forskolin, both in the absence and presence of corticosteroids [24].

Regulatory relationships of AVP

• Cortisol attenuated (p < 0.05) the neuropeptide-induced increases in POMC mRNA, though AVP-stimulated POMC mRNA levels were significantly higher than in cells treated with cortisol alone [25].

Other interactions of AVP

• AVP treatment significantly increased the percentage of irACTH- and POMC-secreting cells in nonpregnant, but not in pregnant, ewes [26].
• This study was designed to test the hypothesis that cardiac receptors tonically inhibit the secretion of renin, arginine vasopressin (AVP) and adrenocorticotropic hormone (ACTH) in late-gestation fetal sheep [27].
• Cell blot analysis of individual corticotrophs identified two types of secretory responses (increases in the number of secreting cells and average amount of ACTH released per cell) to CRH or AVP that changed during fetal development [16].
• AVP, NT and OT failed to release prolactin in ovariectomized ewes [28].

Analytical, diagnostic and therapeutic context of AVP

• 4. The natriuresis induced by intravenous hypertonic NaCl load could be blocked by lowering CSF Na+ concentration in situations where water diuresis was either prevented or reduced by intravenous infusion of AVP or by delayed intracerebroventricular infusion of low-Na+ CSF, respectively [21].
• 1. The antipyretic effect of arginine vasopressin (AVP) introduced into the brain by push-pull perfusion was investigated in the sheep [12].
• Therefore, we examined the control of irACTH secretion by IL cells, whether the responsiveness of AP and IL cells to arginine vasopressin (AVP) and CRH changes during gestation, and whether withdrawal of adrenal steroids by adrenalectomy influences AP and IL responses [29].
• The results suggest that the effect of ovariectomy on the ACTH response to stress occurs at a site within the brain and does not involve altered pituitary responsiveness to CRF or AVP [13].
• The plasma sodium, osmolality, and arginine vasopressin (AVP) responses to phlebotomy, hypertonic saline, water loading and fluid restriction were studied in 2--49 day old lambs [6].

References