Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The corticotropin-releasing effect of arginine-8-vasopressin (AVP) has been compared to that of 1-deamino-8-D-arginine-vasopressin (dDAVP) in male rats of R-Amsterdam strain. AVP increased the level of ACTH and corticosterone in the peripheral blood in a dose-dependent manner. In contrast to AVP, a very potent antidiuretic agent dDAVP which is devoid of pressor activity had no effect on ACTH release and did not stimulate the secretion of corticosterone. It is concluded that CRF activity of vasopressin in vivo is related to its pressor activity. These data are in agreement with the previous findings of these authors demonstrating that dDAVP shows a very low affinity for vasopressin receptors of the cell membranes in the adenohypophysis.
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PMID:Effects of arginine-8-vasopressin and 1-deamino-8-D-arginine-vasopressin on ACTH secretion in rats. 630 4

The present paper reports new findings concerning interaction of [3H]-Arginine-vasopressin with putative receptors in rat anterior pituitary gland. It shows the presence of a single type of receptor sites, with a limited binding capacity and a dissociation constant of nearly 1nM. The parent neurohormone oxytocin revealed weak affinity as compared with vasopressin [Ki = 100nM and Ki = 1nM, respectively]. None of the various peptides tested and, especially corticotropin-releasing factor CRF, competed for binding. Receptor characteristics appeared to be unaffected by lack of circulating vasopressin in Brattleboro rats presenting complete deficiency in synthesis of that peptide.
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PMID:Characterization of specific receptors for vasopressin in the pituitary gland. 631 81

We have investigated the effects of synthetic oxytocin and vasopressin on corticotropin release induced by the 41-residue ovine corticotropin-releasing factor (oCRF) in vitro. Segments of the anterior pituitary glands obtained from male and female Wistar or from female hetero- and homozygous Brattleboro rats were used. Ovine CRF (0.1-2.5 nmol/l) stimulated corticotropin release by pituitaries of Wistar rats and this effect was augmented two- to threefold in the presence of arginine vasopressin (0.09-0.9 mIU/ml) or oxytocin (0.9-90 mIU/ml). A similar phenomenon was demonstrated in Brattleboro rats. These data favor the hypothesis that oxytocin might have a physiological role in the regulation of pituitary-adrenocortical function in homozygous Brattleboro rats which lack vasopressin.
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PMID:Oxytocin as well as vasopressin potentiate ovine CRF in vitro. 631 91

The effects of ovine CRF, lysine vasopressin (LVP), and their interrelationships, and rat hypothalamic extract (HME), on ACTH and beta-endorphin release by human pituitary tumor cells from two patients with Nelson's syndrome and one with Cushing's disease and on ACTH and cortisol secretion in vivo were studied. In cultured pituitary tumor cells, both LVP and CRF greatly stimulated ACTH and beta-endorphin release at maximally active concentrations of 0.1 microM and 10 nM, respectively. At these concentrations, the combination of the two substances had an additive or synergistic effect on hormone release. Low concentrations of HME potentiated and/or were synergistic with CRF-mediated ACTH release. In vivo, the combination of CRF (1 microgram/kg) and LVP (10 pressor units) induced greater ACTH release than the sum of the responses to CRF and LVP alone. This synergistic effect of CRF plus LVP concerned only ACTH release, while cortisol release after CRF plus LVP was equivalent to the sum of the maximal increments in this hormone after CRF and LVP alone. The peak levels of cortisol after a combination of CRF and LVP probably reflect the maximum stimulatory capacity of the adrenal cortex. These data support the concept that in man, both ovine CRF and vasopressin are corticotropin-releasing factors which act synergistically. Both substances might well regulate, at the pituitary level, the responsiveness of the pituitary-adrenal axis to stimuli reaching the hypothalamus. A test using ovine CRF and LVP together might provide a better index of total pituitary ACTH reserve than one using the two compounds separately.
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PMID:Corticotropin-releasing factor (ovine) and vasopressin exert a synergistic effect on adrenocorticotropin release in man. 631 46

Recent studies from our laboratory indicate a primary central site of action of Angiotensin II (AII) to release ACTH. The present studies were designed to test whether AII is able to release ACTH in vivo in a similar fashion in intact, cannulated, freely moving Long-Evans (LE) or in vasopressin (AVP)-deficient, Brattleboro (DI) female rats. The in vivo response to AII was compared with that elicited by synthetic CRF. AII injected i.v. (0.4 or 2 micrograms/100 g BW) induced a significant, dose-related increase in plasma ACTH values 5 and 15 min after injection, in both LE and DI rats. CRF given to LE and DI rats at 0.4 micrograms/100 g BW elicited a larger increase in ACTH plasma values than a similar dose of AII, 5 or 15 min after the injection. Moreover, ACTH levels after CRF in DI rats were significantly greater than those obtained in LE controls. In vitro studies using dispersed anterior pituitary cells indicate that the response of cells from either LE or DI rats to AII or AVP (both at 10(-9) and 10(-8)M) was similar. Cells from DI donors were hyperresponsive to CRF (2 X 10(-11) and 10(-10)M) in terms of ACTH release when compared with the response of cells from LE rats. The present results suggest that the presence of AVP is not essential to mediate the central response to AII and that AII may act centrally to stimulate CRF release from the hypothalamus in vivo, which would then enhance ACTH output. The results in the DI rat indicate that the increased response to CRF may be an important compensatory mechanism involved in the regulation of adrenocortical function in the DI rat.
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PMID:Angiotensin II increases ACTH release in the absence of endogenous arginine-vasopressin. 632 71

The secretion of ACTH by corticotrophs in the anterior lobe of the rat pituitary gland is under the stimulatory influence of at least three receptors, namely that for peptidic CRF (corticotropin-releasing factor), vasopressin and alpha 1-adrenergic agents. CRF is a potent stimulator of cyclic AMP accumulation as well as adenylate cyclase activity in the rat adenohypophysis, thus suggesting an important role of cyclic AMP as mediator of CRF action on ACTH secretion. Vasopressin causes a 2-fold increase of the stimulatory effect of CRF on ACTH release in rat anterior pituitary cells in culture. The potentiating effects of vasopressin on CRF-induced ACTH release are accompanied by parallel changes of intracellular cyclic AMP levels. Vasopressin, while having no effect on basal cyclic AMP levels, causes a 2-fold increase in CRF-induced cyclic AMP accumulation without affecting the ED50 value of CRF action. ACTH secretion is also stimulated by a typical alpha 1-adrenergic receptor. Epinephrine causes a marked stimulation of ACTH release which is additive to that of CRF. Epinephrine, in analogy with vasopressin, although having no effect alone on basal cyclic AMP levels, causes a marked potentiation of CRF-induced cyclic AMP accumulation. Glucocorticoids cause a near-complete inhibition of epinephrine-induced ACTH secretion within 4 h with the following order of ED50 values: triamcinolone acetonide (0.2 nM) greater than dexamethasone (1.0 nM) much greater than cortisol (11 nM) greater than corticosterone (22 nM). Similar effects are observed for CRF- and vasopressin-induced ACTH release. Although the activity of the pituitary-adrenocortical axis in the rat is highly dependent upon sex steroids, 17 beta-estradiol, 5 alpha-dihydrotestosterone and the pure progestin R5020 have no detectable effect on basal or epinephrine-induced ACTH release, thus illustrating the high degree of specificity of glucocorticoids in their feedback control of ACTH secretion. Moreover, glucocorticoids have no effect on CRF-induced cyclic AMP accumulation, thus indicating that their inhibitory effect is exerted at a step following cyclic AMP accumulation.
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PMID:Interactions between CRF, epinephrine, vasopressin and glucocorticoids in the control of ACTH secretion. 632 61

Vasopressin analogs, which markedly differed in the ratio of pressor versus antidiuretic activity and also in ACTH/beta-endorphin-releasing activity, were used in the present study. The ability of vasopressin and these analogs to enhance the release of adrenocorticotropin-(ACTH-IR) and beta-endorphin-like immunoreactivity (beta-EI) induced by synthetic ovine corticotropin-releasing factor -CRF-(1-41)- was studied in vitro using incubated rat anterior pituitary quarters. Arginine vasopressin (AVP) potentiated the action of CRF-(1-41) 2- to 4-fold. Vasopressin analogs, which possess direct CRF-like activity when given alone, also enhanced beta-EI release caused by CRF-(1-41); the lowest concentration able to potentiate CRF-(1-41) activity was closely correlated with the ED50 value of these analogs for direct CRF-like activity. The vasopressin analog 1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)-2-(O-methyl)tyrosine-8-arginine-vasopressin blocked the release of ACTH-IR induced by AVP; however, this analog failed to prevent the potentiation by AVP of ACTH-IR release caused by CRF-(1-41), but enhanced itself the action of CRF-(1-41). Two analogs, which exhibited no direct CRF-like activity and which also did not antagonize the CRF-like activity of AVP, markedly enhanced the ACTH-IR and beta-EI response to CRF-(1-41).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Stimulation of adrenocorticotropin/beta-endorphin release by synthetic ovine corticotropin-releasing factor in vitro. Enhancement by various vasopressin analogs. 632 45

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

Control of the secretion of ACTH appears to involve several mechanisms. It is dependent upon the release, from neurones in the hypothalamus, of corticotrophin releasing factor, which is probably a complex including CRF-41 and vasopressin. The secretion of the complex is influenced by various central inhibitory and excitatory nervous pathways. The releasing factor is conveyed by the hypophyseal portal vessels to the adenohypophysis where it stimulates the secretion of ACTH. The corticosteroids exert a profound control over the basal secretion of ACTH, but only modulate the pituitary adrenocorticotrophic response to stress. The mechanisms which may be involved are summarized in figure 8.
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PMID:The hypothalamo-pituitary-adrenocortical system. 632 52

The ability of the neurohypophyseal hormones and related synthetic peptides to potentiate the action of synthetic ovine corticotropin releasing factor (CRF-41) was examined using male rats whose endogenous CRF release was blocked with chlorpromazine, morphine and nembutal. CRF potency was clearly related to the pressor activity of the analogues. However, the threshold dose for eliciting a significant corticosterone response with the neurohypophyseal hormones was greater than with CRF-41. When arginine vasopressin (AVP) was coadministered with CRF-41 at subthreshold doses of both peptides, a significant corticosterone response was observed. When the neurohypophyseal hormone analogues were compared with regard to intrinsic CRF bioactivity, it was observed that an L-basic residue in sequence position 8 is necessary for high intrinsic activity. With one exception, l-Deamino-(9-D-Ala) arginine vasopressin, the ability to potentiate the effect of CRF-41 was related to the intrinsic CRF potency of the analogues. These results support previous reports of in vitro potentiation of CRF-41 by AVP and point out the complexity of CRF-neurohypophyseal hormone interaction in vivo.
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PMID:In vivo potentiation of corticotropin releasing factor activity by vasopressin analogues. 633 65


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