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 effects on coeliac and superior mesenteric blood flows of intravenous bolus doses of arginine-8-vasopressin (0.7 and 7.0 pmol) porcine neuromedin U-25 (0.01 and 1.0 nmol), rat alpha-calcitonin gene-related peptide (0.05 and 0.5 nmol), bombesin (0.06 and 0.6 nmol), and rat corticotropin-releasing factor (1.0 and 5.0 nmol) were investigated in conscious, Long-Evans rats chronically instrumented with pulsed Doppler flow probes. The peptides investigated were chosen on the basis of the range (vasoconstrictor-vasodilator) of their effects on superior mesenteric blood flow. With the exception of rat corticotropin-releasing factor (which increased coeliac and superior mesenteric flows) all peptides caused directionally opposite changes in coeliac and superior mesenteric blood flows. The results are consistent with the proposition that endogenous neuropeptides could influence blood flows to different abdominal viscera selectively.
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PMID:Differential effects of neuropeptides on coeliac and superior mesenteric blood flows in conscious rats. 221 3

In conscious unrestrained Long-Evans rats, chronically instrumented with miniaturized pulsed Doppler flow probes, intravenous administration of porcine neuromedin U-8 by bolus (0.1 and 1.0 nmol) or infusion (1 and 10 nmol/h) exerted potent constrictor effects on the superior mesenteric vascular bed. With the choice of an appropriate dose, the reduction in superior mesenteric blood flow was not accompanied by any changes in systemic arterial blood pressure, heart rate, and renal or hindquarters blood flows. Porcine neuromedin U-25 had similar effects to neuromedin U-8, but was generally more potent. In Brattleboro rats the pattern of response to neuromedin U-25 was similar to that seen in Long-Evans rats, indicating that mesenteric vasoconstriction was not dependent on release of endogenous vasopressin. In Long-Evans rats the regional hemodynamic actions of rat neuromedin U were comparable with those of porcine neuromedin U-25. The latter peptide at a dose of 1.0 nmol caused a rise in total peripheral resistance and a reduction in cardiac output, with an inconsistent change in heart rate. The results raise the possibility that the high concentration of neuromedin U in the rat intestine is associated with the control of local blood flow.
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PMID:Regional hemodynamic effects of neuromedin U in conscious rats. 230 45

G-protein coupled receptors (GPCRs) are ancient, ubiquitous sensors vital to environmental and physiological signaling throughout organismal life. With the publication of the Drosophila genome, numerous "orphan" GPCRs have become available for functional analysis. Here we characterize two groups of GPCRs predicted as receptors for peptides with a C-terminal amino acid sequence motif consisting of -PRXamide (PRXa). Assuming ligand-receptor coevolution, two alternative hypotheses were constructed and tested. The insect PRXa peptides are evolutionarily related to the vertebrate peptide neuromedin U (NMU), or are related to arginine vasopressin (AVP), both of which have PRXa motifs. Seven Drosophila GPCRs related to receptors for NMU and AVP were cloned and expressed in Xenopus oocytes for functional analysis. Four Drosophila GPCRs in the NMU group (CG14575 [corrected], CG8795, CG9918, CG8784) are activated by insect PRXa pyrokinins, (-FXPRXamide), Cap2b-like peptides (-FPRXamide), or ecdysis triggering hormones (-PRXamide). Three Drosophila GPCRs in the vasopressin receptor group respond to crustacean cardioactive peptide (CCAP), corazonin, or adipokinetic hormone (AKH), none of which are PRXa peptides. These findings support a theory of coevolution for NMU and Drosophila PRXa peptides and their respective receptors.
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PMID:Identification of G protein-coupled receptors for Drosophila PRXamide peptides, CCAP, corazonin, and AKH supports a theory of ligand-receptor coevolution. 1217 21

Recently, novel peptides have been identified as unknown ligands of orphan G-protein coupled receptors. In the paraventicular (PVN) and supraoptic nuclei (SON), the expression of the G-protein genes are abundant. In this review, we focus on the physiological role of neuromedin U and galanin-like peptide, which were recently identified as ligands of G-protein coupled receptors, in the regulation of neurohypophysial hormones. Intracerebroventricular (i.c.v) administration of neuromedin U induced the expression of c-fos mRNA in both the magnocellular and parvocellular division of the PVN and throughout the SON. Administration of i.c.v. neuromedin U caused a significant increase in plasma concentrations of vasopressin and oxytocin as well as adrenocorticotropic hormone. The expression of galanin-like peptide mRNA was observed in the pituicytes of rat posterior pituitary gland. The expression of galanin-like peptide mRNA in the posterior pituitary gland was markedly increased after dehydration, salt loading and intraperitoneal administration of lipopolysaccaride, challenges that stimulate the secretion of vasopressin and oxytocin, and which activate the hypothalamic-pituitary adrenal axis. These results suggest that neuromedin U and galanin-like peptide may have an important role in the regulation of both the hypothalamic-neurohypophysial system and the hypothalamic-adrenohypophysial system.
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PMID:Novel G-protein coupled receptor ligands and neurohypophysial hormones. 1508 78

We have characterized the neuromedin U (NMU)-sensitive neurons in the rat paraventricular nucleus (PVN) using whole-cell patch-clamp recordings and single-cell reverse transcription-multiplex polymerase chain reaction (single-cell RT-mPCR). Following completion of whole-cell recording, the NMU-sensitive neurons were examined for oxytocin (OT), vasopressin (VP), and corticotrophin-releasing hormone (CRH) mRNA expression using single-cell RT-mPCR. Of the NMU-sensitive neurons (n=23), 82% expressed OT mRNA, 9% expressed VP mRNA, 9% did not express the detected specific phenotypes mRNA. Further, the NMU-sensitive neurons (23/23) predominantly expressed NMU-receptor 2 (NMUR-2) mRNA, co-expressed HCN1 channel mRNA, HCN2 channel mRNA, and HCN3 channel mRNA but not HCN4 channel mRNA. These results suggest that NMU modulates the function of the PVN putative parvocellular neurons and is involved in the regulation of OTergic and VPergic neurons by enhanced HCN ion channels activity via NMU-receptor 2.
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PMID:Neuromedin U receptor-2 mRNA and HCN channels mRNA expression in NMU-sensitive neurons in rat hypothalamic paraventricular nucleus. 1563 99

The appetite-suppressive action of brain-gut peptides is similar in both chickens and mammals. In mammals, the brain-gut peptide neuromedin U (NMU) suppresses food intake via hypothalamic neuropeptides, corticotropin-releasing factor (CRF), oxytocin, and arginine-vasopressin. In chickens, central administration of CRF, oxytocin, or arginine-vasotocin (AVT, a nonmammalian equivalent of arginine-vasopressin) suppresses food intake. However, the anorexigenic action of NMU in chickens has not yet been identified. In the present study, we analyzed the effects of the central administration of NMU on food intake and hypothalamic mRNA levels of CRF, AVT and mesotocin (a nonmammalian equivalent of oxytocin) in chicks. Intracerebroventricular administration of NMU in chicks significantly suppressed food intake and induced wing-flapping behavior. NMU also significantly upregulated mRNA expression of CRF and AVT, but did not influence mRNA expression of mesotocin in the hypothalamus. These results suggest that NMU functions as an appetite-suppressive peptide via CRF and AVT in the central nervous system in chicks.
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PMID:Central administration of neuromedin U suppresses food intake in chicks. 1744 84

We recently identified neuromedin S (NMS) as an endogenous ligand for the FM-4/TGR-1 receptor. Here, we examined the possible involvement of central NMS in regulation of urinary output and vasopressin (AVP) release in rats. Intracerebroventricular (icv) injection of NMS induced a dose-dependent increase in the plasma level of AVP, followed by a decrease of nocturnal urinary output. Expression of cFos after icv injection of NMS was observed in the supachiasmatic nucleus (SCN), arcuate nucleus, paraventricular nucleus (PVN), and supraoptic nucleus (SON). The cFos expressing cells in PVN and SON, but not SCN, were then double-stained using antibodies against the vasopressin. On the other hand, icv injection of neuromedin U, which also binds to the FM-4/TGR-1 receptor, required a concentration ten times higher than that of NMS in order to exert the same antidiuretic potency. These results suggest that central NMS may exert a physiological antidiuretic action via vasopressin release.
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PMID:Neuromedin S exerts an antidiuretic action in rats. 1764 72