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)

To investigate catecholamine regulation of adrenocorticotropic hormone (ACTH) and vasopressin (VP) release, the relationship of alpha-adrenergic receptor-binding sites to corticotropin-releasing factor (CRF) and VP-containing cell populations within the paraventricular nucleus (PVN) of the hypothalamus was studied. Immunohistochemistry for CRF and neurophysin-vasopressin (NP-VP) was combined with receptor autoradiography. The adrenergic antagonist [3H]-prazosin was used to visualize alpha-1-binding sites and the agonist [3H]-p-aminoclonidine to visualize alpha-2-binding sites. To determine if changes in adrenergic binding accompanied experimentally induced increased activity of CRF- and VP-containing neurons, adrenalectomy was used as a stimulus for CRF release and dehydration as a stimulus for VP release. Quantitative assessment of autoradiograms revealed a greater density of alpha-1- and alpha-2-binding sites over the medial, parvocellular, CRF-containing region of PVN as compared to the lateral, magnocellular, NP-VP-containing region of the nucleus in all animal groups. Following 10 days of dehydration, the density of alpha-1- and alpha-2-binding sites associated with the CRF- and NP-VP-containing regions of PVN decreased. At 14 days postadrenalectomy the density of alpha-2-binding sites associated with CRF- and NP-VP-containing regions of the nucleus decreased, but the density of alpha-1-binding sites was unchanged. Results of this study support the hypothesis that epinephrine and/or norepinephrine regulate the release of ACTH and vasopressin via alpha-1- and alpha-2-adrenergic receptors associated with CRF- and VP-containing somata within the PVN.
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PMID:Relationship of alpha-1- and alpha-2-adrenergic-binding sites to regions of the paraventricular nucleus of the hypothalamus containing corticotropin-releasing factor and vasopressin neurons. 289 48

1. The melanotropin-releasing activity of arginine-vasopressin (AVP), arginine-vasotocin (AVT), oxitocin (OT), mesotocin (MT) and corticotropin-releasing factor (CRF) was studied in the duck using dispersed, perfused pituitary cells and a specific alpha-MSH RIA. 2. Log dose-response curves were obtained for all the peptides ranging from 5 to 100 ng/ml. All peptides behaved as partial agonists compared to duck median eminence extracts (DME). 3. AVT and MT displayed an alpha-MSH releasing capacity of 60% relative to DME whereas all other peptides behaved as weak agonists with less than 15% capacity relative to DME. 4. AVT and CRF when perfused together acted synergistically on alpha-MSH release yielding a dose response line whose slope approximated that of DME. 5. ACTH was cosecreted together with alpha-MSH in all situations studied with an ACTH to alpha-MSH molar ratio of about 10. 6. It is concluded that CRF and neurohypophyseal peptides may be physiological stimulators of both alpha-MSH and ACTH release in aves.
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PMID:The regulation of the corticomelanotropic cell activity in aves. III--Effect of various peptides on the release of MSH from dispersed, perfused duck pituitary cells. Cosecretion of ACTH with MSH. 290 54

Suspensions of rat anterior pituitary cells were exposed to corticotropin-releasing factor (CRF) (5 nM) and various neurohormones (0.002-1000 nM). CRF-induced secretion of ACTH was doubled by 0.1 nM arginine vasopressin (AVP), 0.2 nM arginine vasotocin, 1 nM oxytocin, 10 nM angiotensin II, and 100 nM noradrenalin; vasoactive intestinal peptide had no effect at 0.2-200 nM. CRF potentiation by AVP was also observed at lower concentrations of CRF. Since AVP appeared to be the most potent modulator of CRF-induced ACTH secretion, potentiation was further tested with specific antidiuretic and oxytocic agonists. Potentiation was clearly related to pressor biological activity, less so to antidiuretic, and hardly at all to oxytocic activities. However, even at 200 nM, the antipressor antagonists dPTyr(Me)AVP and d(CH2)5Tyr(Me)AVP had no effect on potentiation by AVP. The lack of antagonism was partly due to the agonistic effects of the antagonists on the pituitary gland, an effect not observed within vascular tissue. The results thus suggest that anterior pituitary vasopressin receptors resemble, but are not identical to, V1 (pressor and hepatic), do not resemble the V2 (renal), and might be classified as V3 (pituitary) receptors.
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PMID:A novel type of vasopressin receptor on anterior pituitary corticotrophs? 298 63

Specificity of binding of 3H-labeled arginine vasopressin [( 3H]AVP), down-regulation of receptors, and desensitization were studied in anterior pituitary glands of both Wistar and Brattleboro rats. Studies using both crude membrane fractions and isolated cells of anterior pituitaries revealed the presence of a single population of binding sites with a Kd of approximately 1 nM. The receptor recognized the following peptides, with AVP = lysine vasopressin = vasotocin greater than oxytocin = 1-deamino-(8-D-AVP) greater than d-(CH2)5-Tyr-(Me)-Val4-AVP greater than 1-deaminopenicillamine-(Val4-D-Arg8)VP. Neither corticotropin-releasing factor (CRF) nor any of the neuropeptides tested, including AVP ring and tail fragments, competed for tracer binding. Increased extracellular vasopressin levels due to chronic injections or long term adrenalectomy decreased receptor density by 80%, while oxytocin was less effective than AVP. Comparing binding data in Brattleboro homozygotes and heterozygotes revealed that AVP levels within the physiological range could down-regulate pituitary receptors as well. This could not be caused by occupation of sites by endogeneous vasopressin, since injection of large doses of peptide decreased tracer binding by less than 10%. Loss of pituitary receptors reduced 1) enhancement by AVP of CRF-induced cAMP accumulation, 2) intrinsic CRF-like activity and 3) synergistic effect of AVP on ACTH secretion elicited by CRF. This study thus provides evidence for the presence of highly specific vasopressin receptors in the anterior pituitary, which may undergo homologous down-regulation and desensitization in terms of cAMP production and ACTH release.
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PMID:Specific receptors for vasopressin in the pituitary gland: evidence for down-regulation and desensitization to adrenocorticotropin-releasing factors. 298 73

To investigate the mechanism by which ACTH secretion is inhibited during hypothermia, hypophysial portal blood was collected from euthermic and hypothermic rats, and the concentrations of corticotropin-releasing factor (CRF), vasopressin (AVP), and oxytocin (OT) were measured by RIA. Whereas CRF levels in portal plasma were not different in the two groups, AVP and OT levels were significantly lower in hypothermic rats. The concentration of AVP and OT in peripheral plasma was also significantly lower in hypothermic rats compared with euthermic controls. The pituitary responsiveness to CRF during hypothermia was tested in vivo and in vitro. In pentobarbital-anesthetized male rats injected iv with 0.1 or 1.0 nmol CRF, the ACTH response was significantly smaller in hypothermic compared with euthermic animals. However, hemipituitaries superfused at 31 C released the same amount of ACTH in response to 1 nM CRF as hemipituitaries superfused at 37 C (31 C, 541 +/- 90 pg; 37 C, 563 +/- 29 pg) despite reduced baseline secretion (31 C, 77 +/- 10 pg/10 min; 37 C, 114 +/- 14 pg/10 min; P less than 0.05). The data suggest that the inhibition of ACTH secretion during hypothermia is mediated by decreased hypothalamic secretion of AVP and OT which in turn decreases the pituitary responsiveness to CRF.
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PMID:Inhibition of corticotropin release during hypothermia: the role of corticotropin-releasing factor, vasopressin, and oxytocin. 298 77

Stress-induced activation of the pituitary-adrenal system appears to be mediated predominantly by hypothalamic neurons containing ovine corticotropin-releasing factor (oCRF) and vasopressin in the region of the paraventricular nucleus (PVN). Other mediators such as catecholamines, serotonin, angiotensin, and "tissue CRF" may also play a role under certain conditions. Several weeks after ablation of the PVN the response to stress is largely restored while the plasma adrenocorticotropin rise normally elicited by adrenalectomy is still strongly inhibited and immunoreactive oCRF is depleted from the stalk-median eminence region.
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PMID:Mechanisms by which stressful stimuli activate the pituitary-adrenal system. 298 36

Among the putative hypothalamic hormones that can influence the release of adrenocorticotropin (ACTH) in vitro, the 41-amino-acid corticotropin-releasing factor, oxytocin, vasopressin, and epinephrine were identified in hypophyseal portal plasma. Measurement of these substances in several situations associated with changes in ACTH secretion provided data consistent with a physiological role for all four hormones and suggested that control of the hypothalamo-hypophyseal-adrenal axis can be accomplished in different ways in response to different types of stimuli.
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PMID:Measurement of hypothalamic corticotropin-releasing factors in hypophyseal portal blood. 298 42

The generation of antiserums against a peptide that has met the criteria predicted for corticotropin-releasing factor (CRF) has allowed the immunohistochemical localization of CRF immunoreactive neurons in the rat brain. Although CRF-stained cells have been found to be widely distributed in the central nervous system, attention has focused on neurons in the paraventricular nucleus of the hypothalamus (PVH), which is now acknowledged to be the principal source for delivery of CRF to the hypophyseal portal system. Some 2000 CRF-stained neurons can be counted in the PVH of the colchicine-treated rat, and there is evidence that enkephalin, PHI, and neurotensin coexist with CRF in subsets of parvocellular neurons. Consistent with the established negative feedback effects of adrenal steroids on CRF production and release, adrenalectomy enhances CRF immunoreactivity in parvocellular neurosecretory neurons in the PVH. In addition, immunoreactive vasopressin can be demonstrated in a majority of CRF-stained parvocellular neurons after adrenalectomy, which suggests a form of plasticity that allows for synergy of the two peptides in stimulating adrenocorticotropin secretion. The effects of adrenalectomy appear to be glucocorticoid-dependent, and specific to these peptides and this cell type. A survey of neural inputs to the hypophyseotropic zone of the PVH suggests potential substrates for the control of CRF release and/or synthesis by interoceptive stimuli, by the limbic region, and by a number of cell groups in the basal forebrain. Finally, CRF may also participate in other (nonadenohypophyseal) modes of regulation that are represented in the PVH. Thus, CRF immunoreactivity has been demonstrated in a discrete subset of oxytocinergic magnocellular neurosecretory neurons that project to the posterior pituitary, and in a small fraction of cells in the parvocellular division that project to cell groups in the brain stem and spinal cord that are associated with the control of autonomic functions.
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PMID:Localization, colocalization, and plasticity of corticotropin-releasing factor immunoreactivity in rat brain. 298 43

Intact handled rats were pretreated with the immunoglobulin G fractions from normal rabbit serum or antisera to ovine corticotropin-releasing factor (CRF) and/or vasopressin and subjected to restraint or formalin stress. The formalin-induced rise in plasma ACTH was reduced to 28% in rats pretreated with anti-CRF, to 53% in those pretreated with antivasopressin, and to 16% in rats given both antibodies. Pretreatment of animals with anti-CRF, antivasopressin, or a combination of both antibodies also attenuated the ACTH response to restraint stress to 13%, 37%, and 12%, respectively, of those in normal rabbit serum-treated rats. Antiserum pretreatment did not reduce the restraint- or formalin-induced rise in plasma PRL in the same animals, however. We conclude, therefore, that both vasopressin and an ovine CRF-like peptide are physiologically relevant peptides involved in stress-induced ACTH release.
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PMID:Stress-induced secretion of adrenocorticotropin in rats is inhibited by administration of antisera to ovine corticotropin-releasing factor and vasopressin. 298 80

The role of corticotropin-releasing factor (CRF) in four model stresses (cold, ether, immobilization, and trauma) was examined in the guinea pig by using passive immunoneutralization with anti-CRF antiserum. Plasma corticotropin levels were measured at various times after exposure to stress, and groups treated with CRF antiserum were compared with those treated with normal rabbit serum. Of the four stresses tested, ether had the most pronounced effect on corticotropin secretion. Treatment with anti-CRF inhibited most of the ether-induced corticotropin secretory response, the difference between the normal serum- and the anti-CRF antiserum-treated groups being significant at 5 and 10 min (P less than 0.01). Corticotropin responses to cold stress in the two groups differed at the 0.05 level of significance at 10 and 20 min. After administration of trauma (leg fracture), a statistically significant difference (P less than 0.01) between the two groups also was evident, albeit only at 20 min. During immobilization, corticotropin levels differed significantly from control only in the normal serum-treated group but not in the anti-CRF-treated group. These findings show that CRF antiserum was effective in reducing corticotropin levels, indicating that CRF has an important role in mediating corticotropin response to stress. The fact that neutralization was incomplete might be due to an inability of the antiserum to sufficiently neutralize the endogenous CRF or, more likely, reflects the contribution of additional mediators, notably catecholamines and vasopressin, of corticotropin release upon stress.
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PMID:Evidence for a role of endogenous corticotropin-releasing factor in cold, ether, immobilization, and traumatic stress. 298 31


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