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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Subcutaneous injection (0.1 - 3.0 mg/kg) of ethylketocyclazocine (EKC; a prototype kappa agonist) resulted in a dose-dependent increase in urine formation in conscious rats. The increase in urine volume was unaccompanied by a corresponding increase in electrolyte excretion; thus, EKC behaved like a "water diuretic." The diuretic activity was completely abolished by naltrexone, an opiate antagonist. Water loading (10 ml/kg) and EKC (0.5 mg/kg) diminished plasma vasopressin levels equally 60 min after treatment. However, urine formation during the 1 st hr was greater in EKC-treated rats than in water-loaded rats. These results suggested that more than one component was responsible for the diuretic activity of EKC. A central effect of EKC on plasma vasopressin and urine volume was not evident. EKC (10 micrograms/rat) when injected s.c. caused diuresis, but was ineffective as a diuretic when injected into the lateral ventricle. EKC was effective in blocking stimulation of vasopressin secretion caused by volume contraction. EKC also blocked vasopressin-stimulated water flow in the toad bladder, a model of the renal distal tubule and collecting duct. We propose that EKC is diuretic by virtue of inhibition of vasopressin secretion and attenuation of the ADH response in the kidney. Both of these actions may be mediated via opioid receptors responsive to kappa agonists and inaccessible from the cerebroventricle.
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PMID:Studies on the nature and mechanism of the diuretic activity of the opioid analgesic ethylketocyclazocine. 612 Oct 47

The peptides corticotrophin releasing factor (CRF), ACTH4-10 and alpha-MSH have previously been shown to be behaviourally and neurochemically active. Using a passive avoidance task, we studied the effects of intra-ventricular administration of these peptides (0, 10 or 100 ng/rat) given either immediately following the learning trial, or 1 h prior to retention (24 h post-learning) test. We found that they affected behaviour; in some cases improving and in others disrupting performance. Statistical examination of the data suggests that these substances probably act on arousal mechanisms, in a manner reminiscent of the effects of vasopressin [13, 15].
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PMID:Corticotrophin releasing factor is more potent than some corticotrophin-related peptides in affecting passive avoidance behaviour in rats. 630 81

The biological activity of partially purified bovine hypothalamic CRF (corticotrophin- releasing factor) was compared to those of synthetic CRFs (ovine, rat) sauvagine and vasopressin in vivo and in vitro. ACTH-primed hypophysectomized rats with heterotopically transplanted pituitaries and medial basal hypothalamic ablation (H-T + MBHA ), and intact rats pre-treated with chlorpromazine, morphine and Nembutal (C-M-N) were used for in vivo CRF assays. Perifused rat adenohypophyseal fragments were employed for in vitro studies. CRF-A (void volume fractions, 'big' CRF) and CRF-B (Kav = 0.583) purified from bovine hypophyseal stalk, synthetic ovine and rat CRF, and sauvagine all induced significant stimulation of ACTH and/or corticosterone secretion in these systems. Synthetic ovine and rat CRF and sauvagine showed comparable CRF potency. The CRF dose-response slopes for bovine CRF were somewhat steeper than those for ovine CRF or sauvagine in the in vitro system. Vasopressin had the least steep dose-response slope. Intravenous bolus administration of ovine CRF caused a more prolonged (greater than 20 min) elevation of plasma ACTH compared to a relatively short duration after bovine CRF-A. These data suggest that bovine hypothalamus contains substance(s) which exhibits different CRF characteristics from those of ovine CRF.
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PMID:In vivo and in vitro comparisons of biological activities of bovine, ovine and rat CRF (corticotrophin-releasing factor). 632 21

The effect of the non-opiate beta-endorphin (beta E) fragment 2-9 and related peptides on immunoreactive (IR) arginine8 -vasopressin (AVP) levels was studied in the rat eye plexus plasma. Additionally, the effect of beta E 2-9 on AVP release from pituitary neurointermediate lobes ( NILs ), in vitro was studied. IR AVP levels in the eye plexus plasma increased after subcutaneous (s.c.) injection of beta E 2-9. In female rats peak values were observed 2 min after the administration of beta E 2-9 (10 micrograms/rat). Male rats were 100 times more sensitive than female rats. A dose-response study revealed a U-shaped relationship for this effect of beta E 2-9 in animals of both sexes. From structure-activity studies it appeared that beta E 2-9 was the most effective fragment. Intracerebroventricular (i.c.v.) administration of beta E 2-9 did not affect the IR-AVP levels in eye plexus plasma. Moreover, AVP release from the rat NILs cells in vitro was stimulated by perfusion with beta E 2-9, indicating a direct effect of the peptide on the pituitary. Therefore we suggest that beta E 2-9 increases AVP release by a direct action on the posterior pituitary.
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PMID:The stimulatory effect of a non-opiate beta-endorphin fragment on arginine-vasopressin release in rats. 633 Jun 64

Adult male rats were implanted with transcutaneous ECG electrodes and habituated to a dark chamber with elevated background noise levels. ECG was recorded prior to, immediately after, and 3 min after sudden elimination of background noise. The orienting response to the stimulus offset was accompanied by transient bradycardia. Neither AVP (1 microgram/rat) nor oxytocin (1 microgram/rat) injected subcutaneously 1 hr prior to testing altered baseline heart rate or the immediate bradycardiac response to stimulus offset. However, AVP, and to a lesser extent oxytocin, prolonged the bradycardia induced by stimulus offset. The results show that neurohypophyseal peptide hormones enhance the cardiovascular component of orienting to stimulus change.
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PMID:Vasopressin prolongs bradycardiac response during orientation. 646 69

The effect of endogenous vasopressin on the baroreceptor reflex has been examined by comparing baroreflex function in Brattleboro rats with hereditary hypothalamic diabetes insipidus (DI rat) with that in Long-Evans rats (LE rat). Baroreflex function was assessed in conscious unrestrained rats during increases in blood pressure with phenylephrine. The slope of the baroreflex function line in LE rats [(19.0, s.e.m. = 1.4) X 10(-4), n = 34] was significantly steeper than that in DI rats [(6.9, s.e.m. = 0.6) X 10(-4), n = 44, P less than 0.0001]. A subpressor infusion of arginine8-vasopressin (2 ng/kg per min for 2 h i.v.) and an equidose of DDAVP caused bradycardia and increased the baroreflex function slope significantly. Acute volume expansion in DI rat did not change the baroreflex sensitivity. A specific vasopressin vascular receptor antagonist, d(Ch2)5Tyr(Me)AVP, did not alter the baroreflex sensitivity in LE rats. These results suggest that endogenous vasopressin is an important physiological regulator of the baroreflex sensitivity in normal rats.
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PMID:Endogenous vasopressin modulates the baroreflex sensitivity in rats. 662 42

It has been suggested that arginine-vasopressin (AVP) enhances cognitive, and especially mnemonic, ability. Most studies have employed shock avoidance paradigms; we report the results of a study in which saline or vasopressin (0, 0.5 or 1 microgram, mcg, per rat, subcutaneous) pre-treated rats learned to press a lever for food reward. AVP was found to have a disruptive effect on aquisition, particularly when the tendency for these rats to produce extreme learning scores was taken into account. Locomotor activity, with and without vasopressin pre-treatment (0, 0.5, 1 or 2 mcg/rat), was also studied. Only the highest dose significantly reduced activity; therefore, the effects of AVP on acquisition are unlikely to have been caused by motor disruption. The results are discussed in terms of an hypothesis which suggests that AVP enhances arousal, hence influencing performance.
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PMID:The effects of vasopressin on positively rewarded responding and on locomotor activity in rats. 666 21

Infusions of carbachol into the posterior region of the 3rd ventricle of rats for 7 days produced a sustained elevation of blood pressure and heart rate at doses of 0.6 and 1.2 microgram/hr, but only transient rises in blood pressure were obtained at 2.4 microgram/hr. Carbachol, at 0.6 microgram/hr, increased water consumption. At 1.2 microgram/hr, the dipsogenic effect was observed in 50% of the animals and at 2.4 microgram/hr there was no significant change in drinking. Plasma vasopressin levels, measured by radioimmunoassay, were increased by 19-fold 3 min after acute i.c.v. administration of carbachol (0.5 microgram/rat). However, in rats infused with carbachol for 2 or 5 days, the vasopressin levels were not significantly different from controls. The pressor responses to acute and chronic administration of carbachol could be ascribed to the stimulation of periventricular muscarinic receptors because the effects were blocked by atropine, but not by hexamethonium. In carbachol-infused animals, the pressor responsiveness to i.v. norepinephrine and vasopressin were unchanged. From studies using phentolamine, chlorisondamine and a specific vasopressin vasopressor antagonist, it could be inferred that the pressor responses to acute i.c.v. injections of carbachol were due to increased sympathetic activity and vasopressin release. However, the sustained hypertension produced by chronic infusion of carbachol was due primarily to increased sympathetic activity and not to increased plasma levels of vasopressin.
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PMID:Mechanisms underlying the pressor responses to acute and chronic intraventricular administration of carbachol in the rat. 669 15

Rats were tested in a simple one-trial water-finding task for the effects of arginine vasopressin (AVP) on performance of an appetitive task. On the training day, each animal was exposed for 5 min to a novel open-field environment that contained a water-tube located in an alcove set into one of the walls of the enclosure. Immediately upon removal from the enclosure, the animals received a subcutaneous injection of either AVP (1 microgram/rat) or vehicle solution. When water-deprived and tested 48 hr later, vasopressin-treated rats found the water tube reliably faster than controls. In other groups of animals, this potentiation in learned performance was prevented by concurrently treating the rats with a vasopressin analog having potent pressor antagonist properties. These results are consistent with the notion that vasopressin may play a role in memory consolidation, but peripheral visceral factors may mediate this action.
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PMID:Vasopressin potentiation in the performance of a learned appetitive task: reversal by a pressor antagonist analog of vasopressin. 686 69

Systemic injection or arginine vasopressin (AVP) (1 micrograms/rat) significantly prolonged extinction of a pole-jump, active avoidance response in rats; lateral ventricular injection of 1000-fold less AVP (1 ng/rat) produced similar results. A new AVP analogue, [1-deaminopenicillamine-2-(O-methyl)tyrosine]arginine vasopressin (dPTyr-(Me)AVP), is known to antagonize behavioral and vascular effects of exogenous AVP at molar ratios of 5 : 1. At a dose of 100 micrograms/rat (subcutaneously) dPTyr-(Me)AVP produces, by itself, a behavioral effect opposite to that of exogenous AVP, namely a facilitation of extinction. Injections of dPTyr-(Me)AVP into the lateral ventricle were ineffective except at a dose of 10 micrograms/rat. These results confirm previous reports of the effect of vasopressin on delaying extinction of avoidance behavior, but suggest a site of action distant from the lateral ventricle.
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PMID:Arginine vasopressin and a vasopressin antagonist peptide: opposite effects on extinction of active avoidance in rats. 725 68


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