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)

Histamine (HA) stimulates the release of the pro-opiomelanocortin (POMC)-derived peptides ACTH, beta-endorphin (beta-END), beta-lipotropin and alpha-melanocyte-stimulating hormone, and HA is involved in the mediation of the stress-induced release of these peptides. The effect of HA is indirect and may involve the hypothalamic regulating factors, corticotropin-releasing hormone (CRH) and/or arginine-vasopressin (AVP). We studied the effect of immunoneutralization with specific antisera against CRH or AVP on the response of ACTH and beta-END to HA, restraint stress, CRH, AVP or a posterior pituitary extract in male rats. Intracerebroventricular infusion of HA (34-540 nmol) increased the plasma levels of ACTH and beta-END immunoreactivity (beta-ENDir) in a dose-dependent manner. Pretreatment with antiserum to CRH or AVP prevented the ACTH response to 270 nmol HA and inhibited the beta-ENDir response by 30-60%. One to five minutes of restraint stress caused an increase in the plasma levels of ACTH and beta-ENDir. The increase was dependent on the duration of stress exposure. Pretreatment with CRH antiserum abolished the ACTH response to 5 min of restraint stress and inhibited the beta-ENDir response by 60%. Immunoneutralization with AVP antiserum had only half the inhibitory effect of that seen with CRH antiserum. CRH (100 pmol i.v.) increased the plasma levels of ACTH and beta-ENDir. This effect was abolished by pretreatment with CRH antiserum, whereas pretreatment with AVP antiserum prevented the CRH-induced ACTH release and inhibited the beta-ENDir response by 50%. AVP (24-800 pmol i.v.) stimulated ACTH and beta-ENDir in a dose-dependent manner. CRH and AVP antisera each prevented the effect of AVP (800 pmol) on ACTH secretion, whereas the beta-ENDir response to AVP was only inhibited by about 60% by the antisera. An extract of the posterior pituitary gland administered in a dose corresponding to 0.15 or 0.5 pituitary equivalents had no effect on ACTH secretion, while 1.0 pituitary equivalent increased the ACTH concentration in plasma. This effect was abolished by AVP antiserum. The posterior pituitary extract caused a dose-dependent rise in plasma beta-ENDir which might be due to an unavoidable contamination of the posterior pituitary extract by a small amount of beta-END from the intermediate lobe. Consistent with this view, AVP antiserum had no effect on the rise in the plasma concentration of beta-ENDir following administration of the posterior pituitary extract.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Histamine- and stress-induced secretion of ACTH and beta-endorphin: involvement of corticotropin-releasing hormone and vasopressin. 133 40

Corticotropin-releasing hormone (CRH), somatostatin (SOM), delta-sleep-inducing peptide (DSIP), neuropeptide Y (NPY), beta-endorphin (beta-END), and vasopressin (AVP), which are regarded as being involved in the HPA-regulation were investigated in lumbar CSF of 44 suicide attempters. The patients were diagnosed according to the DSM-III-R, and rated with the MADRS. The neuropeptides were compared with the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in CSF and with post-dexamethasone plasma cortisol. We found strong correlations between CRH and the peptides SOM and beta-END. The latter also correlated positively with SOM. There were no differences between men and women. Patients with major depressive disorders had significantly lower SOM, CRH, and DSIP than other patients. Both SOM and beta-END correlated negatively with post dexamethasone plasma cortisol in all patients. We found no significant relationships between neuropeptides and CSF 5-HIAA. Patients who had made previous suicide attempts had significantly lower CRH than those who had not. No other significant associations between neuropeptides and suicidal subgroups of patients appeared, and there was no indication of specific neuropeptide patterns in patients who later completed suicide. Intercorrelations of some neuropeptides and low SOM and DSIP in major depressed patients are findings in line with those by others.
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PMID:HPA-related CSF neuropeptides in suicide attempters. 137 70

The neurotransmitter histamine (HA) participates in the neuroendocrine regulation of pituitary hormone secretion and in the regulation of some peripheral hormones. In general, HA has a stimulatory but indirect effect on the release of these hormones by activation of postsynaptic receptors in the hypothalamic region. The release of the pro-opiomelanocortin-derived peptides ACTH, beta-endorphin (beta-END), and alpha-melanocyte-stimulating hormone (alpha-MSH) occurs by stimulation of H1- and H2-receptors and seems to be mediated via release of corticotropin-releasing hormone and vasopressin from the hypothalamus. The HA-induced release of prolactin (PRL) involves H2-receptors in some hypothalamic areas and H1-receptors in other areas. The release of PRL occurs by histaminergic inhibition of tuberoinfundibular dopaminergic neurons and by stimulation of serotoninergic and vasopressinergic neurons. Histaminergic neurons seem to participate in the mediation of the stress-induced release of ACTH, beta-END, alpha-MSH, and PRL. The neurohypophysial hormones vasopressin and oxytocin are stimulated by HA, and a physiological role of HA in the control of vasopressin secretion is likely. HA stimulates the release of peripheral catecholamines and renin. The stress-induced increase in plasma catecholamines and plasma renin activity (PRA) seems also to involve central histaminergic neurons. The effect of HA and stress on peripheral catecholamines is mediated via H1- and H2-receptors, while that on PRA is mediated via H2-receptors.
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PMID:Neuroendocrine functions of histamine. 205 12

The levels of dynorphin-(1-13), leucine enkephalin, beta-endorphin and vasopressin immunoreactivity (ir-DYN, ir-1-ENK, ir-beta-END, ir-VP) have been determined in the anterior and in the neurointermediate lobes of the pituitary of rats subjected to a variety of manipulations. Dehydration of rats by 5 days enforced inhibition of a 2% solution of NaCl resulted in a significant decrease in the levels of ir-DYN, ir-1-ENK and ir-VP, but not in those of ir-beta-END in the neurointermediate lobe of the pituitary. In contrast, substitution of drinking water by a solution containing 20 microgram/ml dexamethasone for 5 days produced a significant increase in the neurointermediate pituitary content of ir-DYN, ir-1-ENK and ir-VP, whereas levels of ir-beta-END remained unaffected. This treatment, however, resulted in a significant fall in the ir-beta-END content of the adenopituitary without changing levels of ir-DYN in this structure. Adrenalectomy was associated with a significant decrease in the ir-DYN, ir-VP and ir-1-ENK content of the neurointermediate lobe of the pituitary and a pronounced elevation in the ir-beta-END but not ir-DYN content of the adenohypophysis. These observations are indicative that the regulation mechanisms of the functional state of particular endorphins differ between the anterior and neurointermediate lobes of the pituitary. The concomitant alterations in levels of ir-DYN, ir-1-ENK and ir-VP detected suggest that a common or similar mechanism of regulation may exist for these peptides. A common biosynthetic origin, however, appears to be unlikely, since Brattleboro rats which are unable to synthesize vasopressin possess unchanged ir-DYN- and ir-1-ENK- levels in the pituitary.
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PMID:Levels of dynorphin-(1-13) immunoreactivity in rat neurointermediate pituitaries are concomitantly altered with those of leucine enkephalin and vasopressin in response to various endocrine manipulations. 627 85

The ability of arginine8 vasopressin (AVP) to potentiate the beta-endorphin-releasing activity of synthetic ovine corticotropin releasing factor (oCRF) was examined using an anterior-pituitary quarter assay. Both AVP and oCRF stimulated the release of beta-endorphin immunoreactivity (beta-END-I) in a dose-dependent manner, with AVP being approximately 10 times less effective than oCRF. Marked potentiation of beta-END-I release was observed when pituitary quarters were incubated in the presence of a combination of 0.5 nM oCRF and 1.0 nM AVP. Further potentiation was not observed when the higher doses of 1.0 nM oCRF and 2.0 nM AVP were tested in combination; however, maximal beta-END-I release may have been attained by the addition of 1.0 nM oCRF alone. These results suggest that AVP may play a role in the mediation of beta-endorphin release from the adenohypophysis.
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PMID:Arginine8 vasopressin potentiates the beta-endorphin-releasing activity of ovine corticotropin-releasing factor (oCRF) in vitro. 630 71

[he concentrations of immunoreactive (ir-) peptides derived from the opioid peptide precursors proenkephalin A (Met-enkephalin), proenkephalin B [dynorphin (DYN)-(1-17), dynorphin-(1-8), dynorphin B, alpha-neoendorphin (alpha-NEO-E), beta-NEO-E] and proopiomelanocortin [beta-endorphin (beta-END)], and of the neurosecretory hormones vasopressin and oxytocin increased between approximately 10-fold and 50-fold from birth to adulthood in the rate hypothalamus. Gel filtration and HPLC analysis of proenkephalin B-derived opioid peptides revealed that in 3-day-old rats the predominant portion of ir-dynorphin-(1-17) and a substantial part of ir-dynorphin B consisted of a high (6000) mol wt species, a common precursor peptide for DYN-(1-17) and DYN B. In adults rats, however, authentic DYN-(1-17) and DYN B were found to be the major ir-forms. The mol wt patterns of ir-DYN-(1-8), ir-alpha-NEO-E and ir-beta-NEO-E did not differ between 3-day-old and adult rats and reflected predominantly the respective authentic opioid peptides. Taking into consideration the developmental changes in the mol wt pattern of ir-DYN-(1-17), authentic DYN-(1-17) was 5 times lower in concentration than DYN-(1-8) in 3-day-old rats, whereas in adults these opioid peptides occurred in equimolar concentrations. These findings suggest that the posttranslational processing of the precursor proenkephalin B changes in the course of postnatal development. Ir-beta-END in the hypothalamus of newborn and adult rats consisted exclusively of beta-END-sized peptides which were not (unlike those in the intermediate pituitary lobe) alpha-N-acetylated. Thus, in the hypothalamus, the enzymatic processing of the opioid peptide precursor proopiomelanocortin to beta-END seems to be fully active at birth, in contrast to that of proenkephalin B.
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PMID:Evidence for a differential postnatal development of proenkephalin B (= prodynorphin)-derived opioid peptides in the rat hypothalamus. 654 67

We investigated in conscious, male rats (1) whether the role of arginine-vasopressin (AVP) in histamine (HA)- and/or restraint stress-induced stimulation of ACTH and beta-endorphin (beta-END) secretion is mediating and/or permissive and (2) whether AVP possesses a potentiating effect on HA- or stress-induced release of ACTH and beta-END. Administration of a specific V1 receptor agonist stimulated ACTH and beta-END secretion dose-dependently while a V2 receptor agonist had no stimulating effect. ACTH and beta-END secretion was stimulated 2- to 3-fold by intracerebroventricular (i.c.v.) infusion of HA (270 nmol) or by 5 min of restraint stress. These effects were inhibited approximately 80% by immunoneutralization of endogenous AVP using a specific AVP antiserum. When the 'AVP tone' was restored in immunoneutralized animals by administration of the specific AVP V1 receptor agonist, which was not bound by the AVP antiserum and had no ACTH and beta-END-releasing effect in the dose used, the ACTH and beta-END response to HA or restraint stress was almost completely reestablished. The specific AVP V2 receptor agonist, which was not bound by the AVP antiserum, reestablished only in part the response of ACTH and beta-END to HA or restraint stress in immunoneutralized animals. AVP administered in doses which had no or minimal ACTH or beta-END releasing effect in itself enhanced the ACTH or beta-END response to submaximal stimulation with HA or restraint stress.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Permissive, mediating and potentiating effects of vasopressin in the ACTH and beta-endorphin response to histamine and restraint stress. 811 28

Arginine-vasopressin (AVP) seems to be involved in the histamine (HA)-and stress-induced release of ACTH and beta-endorphin (beta-END). We studied the effect of selective AVP V1-or V2-receptor blockade on the ACTH and beta-END response to HA or restraint stress in conscious male rats. HA (270 nmol) administered intracerebroventricularly or 5 min of restraint stress caused a 3-to 7-fold increase in the plasma levels of ACTH and beta-END immunoreactivity (beta-ENDir). Pretreatment of the animals with the nonselective V1+2-receptor antagonist [1-Pmp-2-D-Phe-4-Ile-8-Arg]vasopressin, which was administered intravenously in a low (23 nmol) or a high dose (90 nmol) inhibited the HA-or restraint stress-induced secretion of ACTH and beta-ENDir 60 and 25-70%, respectively. Pretreatment with equipotent doses of the selective V1-receptor antagonist [1-(p-tBu)Pmp-2-Tyr(O-Me)-8-D-Arg]vasopressin (25 nmol) and/or the selective V2-receptor antagonist [1-Pmp-2-D-Ile-4-Ile-8-Arg]vasopressin (7.0 nmol) attenuated the response of ACTH and beta-ENDir to HA or restraint stress by 60-80 and 40-60%, respectively. In general, these doses of antagonists had no effect on basal hormone levels. We conclude that AVP takes part in the mediation of HA- and restraint stress-induced ACTH and beta-END secretion. This effect seems to be mediated via both AVP V1- and V2-receptors or a less selective receptor with ligand specificity for both V1- and V2-receptor antagonists.
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PMID:Involvement of vasopressin V1- and V2-receptors in histamine-and stress-induced secretion of ACTH and beta-endorphin. 839 63

The aim of the present study was to analyze the neurochemical properties of the centrifugal visual system (CVS) of the quail using an immunohistochemical approach by testing 16 neuropeptides (angiotensin: ANG, bradykinin: BK, cholecystokinin, dynorphin, L and M-enkephalin, beta-endorphin: beta-END, galanin, alpha-neoendorphin, neurokinin A, neuropeptide Y (NPY), ocytocin, somatostatin, substance P, vasopressin, vasoactive intestinal polypeptide) and three neurotransmitters or their synthetic enzymes (choline acetyltransferase: ChAT, tyrosine hydroxylase: TH, serotonin: 5-HT and nitric oxide synthase: NOS, including the histochemical nicotinamide adenine dinucleotide phosphate diaphorase technique). For each substance, the somatic and afferent fiber and terminal labeling was analyzed within the nucleus isthmo-opticus (NIO) and the ectopic area (EA) and compared with that of retinopetal cell bodies labeled retrogradely with RITC following its intraocular injection (double-labeling procedure). The results showed that none of the centrifugal neurons were reactive to any of the substances tested. In contrast, all with the exception of ANG, BK and beta-END, labeled fibers and terminals within the EA and only four (ChAT, 5-HT, NPY and NOS) within the NIO. Possible sources of these immunoreactive fibers terminating in the NIO and EA were investigated by mapping the somatic immunolabeling of the different substances within brainstem regions previously shown by Miceli and other authors to project upon the centrifugal neurons. The data suggests that, besides the rapid retino-tecto-NIO-retinal loop, which facilitates the transfer of meaningful or more relevant information within particular portions of the visual field, the multiple afferent input which stems from various brainstem regions utilizes a wide range of neuroactive substances. Some of these afferent projections upon the centrifugal neurons appear to belong to nonspecific systems which might play a role in modulating the excitability of centrifugal neurons as a function of arousal.
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PMID:An immunohistochemical study of putative neuromodulators and transmitters in the centrifugal visual system of the quail (Coturnix japonica). 971 61

The gas nitric oxide (NO) is an important messenger in brain signaling. Along with many other functions, NO is thought to influence the expression and/or release of various hypothalamic hormones (corticotropin-releasing hormone (CRH), gonadotropin-releasing hormone (GnRH) and vasopressin). To learn more about the role of NO in neuroendocrine mechanisms, we studied in mutant mice lacking neuronal isoform of NO synthase (nNOS) the cellular expression of CRH, neurophysin (the carrier protein of vasopressin/oxytocin) and pro-opiomelanocortin (POMC), as well as of the POMC-derived peptides beta-endorphin (beta-END), alpha-melanocyte-stimulating hormone (alpha-MSH) and corticotropin (ACTH) by use of immunohistochemistry and in situ hybridization. Additionally, the remaining NO-generating capacities of the nNOS minus mice were investigated by NADPH-diaphorase histochemistry and citrulline immunohistochemistry as well as by immunohistochemical localization and Western blot analysis of endothelial NOS (eNOS) and nNOS isoforms. Amongst all hypothalamic peptides under investigation, only beta-END was found to be altered in mutant mice. A morphometric analysis of beta-END producing neurons of the arcuate nucleus revealed that significantly less cells were immunoreactive in mutant mice, whereas the expression of the precursor POMC as well as of other POMC-derived peptides was found to be unchanged. In addition to that, fewer beta-END-immunoreactive fibers were found in the paraventricular nucleus of nNOS minus mice in comparison to wild-type animals. Hence, the reduction of hypothalamic beta-END is probably a posttranslational event that might reflect a disturbed endorphinergic innervation of those hypothalamic neurons which normally express nNOS.
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PMID:Expression of hypothalamic peptides in mice lacking neuronal nitric oxide synthase: reduced beta-END immunoreactivity in the arcuate nucleus. 987 4


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