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 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

Since neuroimmunomodulation is brought about in part, at least, by secretion of pituitary hormones involved in stress and immune responses, we review briefly the hypothalamic control of the release of ACTH, growth hormone, and prolactin. The release of ACTH is controlled particularly by corticotropin-releasing factor (CRF), but vasopressin has intrinsic releasing activity and potentiates the action of CRF at both hypothalamic and pituitary levels. Oxytocin may even potentiate the action of CRF, but has little, if any, ACTH-releasing activity by itself. In addition, epinephrine may augment responses to the CRFs. In contrast, growth hormone is under dual control by growth-hormone-releasing factor (GRF) and somatostatin, and prolactin is under multifactorial control by a series of inhibitors and stimulators. Dopamine is accepted as a physiological prolactin-inhibiting factor (PIF), but probably GABA and possibly acetylcholine as well are PIFs. There is good evidence for a peptide PIF as well. There are a number of prolactin-releasing factors (PRFs) which include oxytocin, vasoactive intestinal polypeptide, PHI and TRH. Several other peptides can also release prolactin, including angiotensin II. In response to stress there is a complex interaction of peptides intrahypothalamically. CRF augments its own release by an ultra short-loop positive feedback, and there is negative ultra short-loop feedback of GRF and somatostatin. Vasopressin appears to augment CRF release as well as to act directly on the pituitary, and there are complex interactions of various peptides to influence prolactin and GH release.
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PMID:The role of brain peptides in neuroimmunomodulation. 347 67

Recently two hypothalamic releasing factors have been isolated, sequenced and synthesized: corticotropin-releasing factor (CRF) from sheep and rat hypothalami; and growth hormone-releasing factor (GH-RF) from tumors in human pancreas (hpGH-RF) and from rat hypothalami (rhGH-RF). Their biological potencies were tested by various laboratories in vivo and in vitro using rat pituitary cell cultures and the pituitary quarters method. In the present study, we investigated the dynamics of the release of pituitary hormones and the interaction between CRF and hGH-RF and several brain peptides in a pituitary cell-superfusion system. A dose-related ACTH release was found when the cells were superfused with different doses of synthetic CRF. Synthetic hGH-RF44, hGH-RF40, hGH-RF1-29 and purified porcine hypothalamic GH-RF caused similar dose-related releases of GH. In this system, we demonstrated interactions between CRF and vasopressin, CRF and SP, hGH-RF and vasopressin and hGH-RF and PHI-27. We conclude that the control of pituitary hormone secretion is a complex process; several factors may interact with each releasing or inhibiting factor to modulate their effects.
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PMID:Interaction between hypothalamic peptides in a superfused pituitary cell system. 620 10

Previous studies in our laboratory have demonstrated that PVN administration of equimolar doses of VIP and PHI induce similar increases in plasma ACTH and CORT concentrations via the release of CRF and vasopressin in fasted, freely moving rats studied during the early light cycle. The purpose of these investigations was to determine whether VIP and PHI act via the same receptor and/or mechanism. Individual studies involving the PVN administration of either VIP or PHI in doses ranging from 0.3 to 30.0 nmol/rat demonstrated that VIP increases both ACTH and CORT secretion throughout the administered range. In contrast, PHI was an effective stimulant in doses up to 15 nmol/rat but had no effect on either ACTH or CORT at a dose of 30 nmol/rat thus yielding a bell-shaped dose-response curve. When increasing doses of PHI (0.15-3.0 nmol/rat) were administered against a background of VIP (3.0 nmol/rat) predictably additive responses were observed; however, when increasing doses of VIP (0.15-3.0 nmol/rat) were administered with PHI (3.0 nmol/rat) only the higher doses of VIP facilitated the PHI-induced secretion while the lower doses of VIP actually reduced the PHI-induced ACTH secretion. Finally, pretreatment with [Lys1, Pro2,5, Arg3,4, Tyr6]-VIP, anVIP (1.5 nmol/rat) totally suppressed VIP-induced ACTH secretion but had no effect on PHI-induced secretion. These studies collectively suggest that VIP and PHI utilize different receptors/mechanisms to regulate HPA secretion. Furthermore, when a range of doses of anVIP (1.5-30.0 nmol/rat) was tested against VIP (3.0 nmol/rat), ACTH secretion was totally suppressed at all doses of the antagonist. However, the maximal reduction of CORT secretion occurred at the lowest dose of anVIP and increasing doses were less and less effective, suggesting that not only PHI but VIP may also stimulate and inhibit HPA secretion. While both the stimulatory and the inhibitory actions of PHI appear to involve ACTH, only the stimulatory action of VIP is ACTH-dependent.
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PMID:VIP antagonist demonstrates differences in VIP- and PHI-mediated stimulation and inhibition of ACTH and corticosterone secretion in rats. 857 37

Accumulating evidence indicates that somatostatin (SS) is a key substance for the circadian rhythm of rodents. In the present study, we investigated whether SS mRNA coexists with arginine-vasopressin (AVP) mRNA, vasoactive intestinal peptide/peptide histidine isoleucine amide (VIP/PHI) mRNA and glutamate decarboxylase (GAD) mRNA in neurons of the rat suprachiasmatic nucleus (SCN) by double labeling in situ hybridization technique. SS mRNA-positive neurons were scattered in the whole region of rostral SCN, in the intermediate region between dorsomedial and ventrolateral region at the middle level, and in the mid to lateral region at the caudal level. These neurons were located in the close vicinities of the dorsomedial AVP and ventrolateral VIP/PHI mRNA-positive cell clusters. They rarely coexpressed AVP mRNA or VIP/PHI mRNA, but mostly coexpressed GAD mRNA. Thus, SS-synthesizing neurons are GABAergic and form a distinct cell group different from AVP or VIP/PHI cell groups.
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PMID:Somatostatin neurons form a distinct peptidergic neuronal group in the rat suprachiasmatic nucleus: a double labeling in situ hybridization study. 888 10

The hypothalamic suprachiasmatic nucleus (SCN), the circadian clock in mammals, generates and maintains a variety of daily rhythms. The present review is an attempt to synthesis experimental data on the anatomical organisation and cellular activities within SCN. The clock exhibits an endogenous rhythmic activity and can also be entrained by environmental synchronisers such as the light/dark cycle. It can be also influenced by internal signals such as the rhythmic secretion of melatonin which is under control of SCN activity. This tiny structure contains a variety of peptides organised in a specific distribution. It receives three main inputs from the retina (glutamate), the intergeniculate leaflet (NPY) and the dorsal raphe (serotonin). VIP containing cells located in the ventral part of SCN receive all these afferences and innervate the whole structure. VIP, PHI and GRP are likely implicated in the entrainment of the clock. The vasopressin (VP) cells exhibiting an endogenous rhythmic synthesis are considered as an output of the clock. The specific induction of immediate early genes (c-fos, jun B) within SCN by light pulses during the subjective night suggests the participation of these genes in the process of cellular entrainment by the photic input. The demonstration of a rhythmic astrocytic activity within SCN suggests an active involvement of this cellular population in the functioning of the clock facilitating or not neuronal communication. Cellular disturbances such as a decrease in VIP or VP cell population, reduction in the amplitude of functional cellular rhythms, astrocytic proliferation could explain some pathologies observed with ageing.
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PMID:[The suprachiasmatic nucleus: cellular approach to clock functioning]. 897 7