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)

Regional haemodynamic responses to endothelin-1 were assessed in conscious, unrestrained Long Evans rats, chronically instrumented with pulsed Doppler flow probes. Bolus injection of endothelin-1 (0.04 nmol) caused an early transient hypotension and increase in hindquarters vascular conductance. In the presence of NG-monomethyl-L-arginine (L-NMMA), which inhibits endothelial cell nitric oxide production, the hindquarters vasodilator response to endothelin-1 was unchanged and similar to that seen in the presence of vasopressin when the latter was infused to simulate the pressor effects of L-NMMA. These results indicate that the hindquarters vasodilatation in response to endothelin-1 is not dependent upon release of nitric oxide from endothelial cells.
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PMID:NG-monomethyl-L-arginine does not inhibit the hindquarters vasodilator action of endothelin-1 in conscious rats. 269 39

Three classes of vasodilators mediate their effects through the activation of guanylate cyclase and the increased synthesis of cyclic GMP. Nitrovasodilators such as nitroglycerin, nitroprusside, hydroxylamine, azide, etc. result in the generation of the nitric oxide free radical that activates the cytosolic (soluble) isoenzyme form of guanylate cyclase. These agents have been useful in increasing cyclic GMP synthesis in numerous model systems and these effects are independent of extracellular calcium. The increased synthesis of cyclic GMP and the activation of cyclic GMP-dependent protein kinase result in the altered phosphorylation of many smooth muscle proteins including the dephosphorylation of myosin light chain, which is associated with vascular and tracheal smooth muscle relaxation. These latter effects may result from cyclic GMP decreasing cytosolic free calcium concentrations and the activity of myosin light chain kinase. Another class of vasodilators, designated endothelium-dependent vasodilators, includes a long list of agents such acetylcholine, histamine, A23187, ATP, thrombin, etc. that relax vessels only when the endothelium is intact. These agents result in the increased endothelial synthesis and/or release of a factor(s) designated endothelial-derived relaxant factor (EDRF), the structure of which is unknown. This labile factor also activates the soluble isoenzyme form of guanylate cyclase in the smooth muscle resulting in cyclic GMP accumulation and the same cascade of events as above. There is evidence that even under basal, non-stimulated conditions there is EDRF release that influences vascular tone due to the increased synthesis of cyclic GMP. A third class of vasodilators, atrial natriuretic factor (ANF) or atriopeptins, includes a family of peptides that are produced in cardiac atria and other tissues and influence cardiovascular volume and dynamics by causing natriuresis, diuresis, vasodilation and decreased renin, aldosterone and vasopressin secretion. These peptide hormones also increase cyclic GMP synthesis in vascular, renal, adrenal and other tissues. These effects are mediated through specific ANF receptors that couple to and activate the membrane (particulate) isoenzyme form of guanylate cyclase and increase cyclic GMP-dependent protein kinase activity. There are two ANF receptor subtypes in most cells and tissues that are 130,000 and 66,000 daltons. The ANF receptor of about 130,000 daltons, designated receptor ANF-R1 copurifies with particulate guanylate cyclase through numerous procedures and may be part of the membrane-associated guanylate cyclase complex.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Regulation and role of guanylate cyclase-cyclic GMP in vascular relaxation. 289 Jan 72

Responses to angiotensin II, bradykinin and arginine vasopressin were compared in helical strips of canine pulmonary arteries and veins. Angiotensin II contracted the artery but relaxed the vein strip. The artery contraction was augmented by indomethacin and aspirin and was abolished by losartan. The vein relaxation was not affected by endothelium denudation but was abolished by the cyclooxygenase inhibitors, a prostaglandin I2 synthase inhibitor and losartan. The bradykinin-induced artery relaxation was inhibited by endothelium denudation, NG-nitro-L-arginine (L-NA) or indomethacin and abolished by their combined treatment. The vein relaxation produced by bradykinin was endothelium-independent and was abolished by indomethacin. Vasopressin produced a slight relaxation in the arteries, which was abolished by endothelium denudation and L-NA. The vein relaxation produced by vasopressin was abolished by endothelium denudation and combined treatment with L-NA and indomethacin. It may be concluded that (1) activation of angiotensin AT1 receptor subtype in smooth muscle produces contraction and also relaxation due to prostaglandin I2 release; the former predominates over the latter in the artery, whereas only the latter is operative in the vein, (2) the bradykinin-induced relaxation is due to nitric oxide (NO) from the endothelium and prostaglandin I2 from subendothelial tissues in the artery and solely to prostaglandin I2 in the veins, and (3) the vasopressin-induced relaxation is mediated by endothelial NO in the artery, and NO and prostaglandin I2 in the vein.
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PMID:Comparison of responses of canine pulmonary artery and vein to angiotensin II, bradykinin and vasopressin. 749 82

The effects of two classes of phospholipids (PL) on renal function have been studied. Bolus injections of 1 ng (10 pmol) of lysophosphatidylcholine (LPC) caused natriuresis and diuresis in rats. Natriuretic activity was eliminated by substituting unsaturated bonds in the 1-acyl group and by removing the choline group on the sn-3 position. Natriuretic activity was not affected by substitution of 1-alkyl for 1-acyl groups. In the dog, LPC was natriuretic when given as a bolus of 3.0 micrograms/kg or as a constant infusion at 5 ng/kg/min. To explore further the effect of alkyl PLs on renal function, a series of studies with platelet activating factor (PAF) was performed. PAF injected directly into the renal artery (IR) in bolus doses of 0.5-10 ng/kg caused renal vasodilation that was blocked by a specific PAF receptor antagonist. This effect was not due to release of vasodilatory eicosanoids, dopamine, or nitric oxide (NO). PAF given IR as a continuous infusion at 2.5 ng/kg/min attenuated the renal vasoconstrictor effects of angiotensin II and norepinephrine but not vasopressin. This effect to attenuate vasoconstriction was blocked by the NO inhibitor N-monomethyl-L-arginine. These studies using picomolar amounts of PL suggest a physiologic role for these compounds in control of renal function.
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PMID:Effects of phospholipids on renal function. 750 37

Using pentobarbital-anesthetized euvolemic dogs, we investigated whether vasopressin V2-receptor stimulation induced renal vasodilation and whether nitric oxide (NO) had a role in the process. Intrarenal infusion of arginine-vasopressin (AVP) resulted in renal vasoconstriction with pressor response. After preadministration of a V1-receptor antagonist, however, intrarenal infusion of AVP caused an increase in renal blood flow (RBF) without pressor action, indicating renal vasodilation. This renal vasodilation was not observed when we infused AVP after-simultaneous pretreatment with V1- and V2-receptor antagonists. Even in the absence of the V2-receptor antagonist, this renal vasodilation was attenuated by intrarenal infusion of L-NG-nitroarginine (L-NNA). Concomitant infusion of L-arginine prevented the inhibitory effect of L-NNA on renal vasodilation induced by intrarenal infusion of AVP in the presence of the V1-antagonist. These data indicate that the renal vasodilation caused by intrarenal infusion of AVP in the presence of a V1-antagonist was mediated by V2-receptor stimulation, and the inhibitory effect of L-NNA on V2-receptor-mediated renal vasodilation was attributed to its inhibitory effect on NO synthesis, suggesting that NO may participate in V2-receptor-mediated renal vasodilation.
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PMID:Nitric oxide may participate in V2 vasopressin-receptor-mediated renal vasodilation. 751 66

There is increasing evidence that nitric oxide (NO) plays a role within the central nervous system as a novel messenger. Neuronal culture work suggests NO to be involved specifically in mediating actions of angiotensin II (ANG). The present study examined the potential role of NO within the paraventricular nucleus (PVN), a structure involved in mediating the cardiovascular changes initiated by activation of the subfornical organ (SFO). The pressor response to stimulation of SFO, which can be divided into a short (SD) and long duration (LD) component was enhanced following administration of an NO synthase inhibitor (L-NAME) (SD control: 101 +/- 4 vs. post L-NAME: 145 +/- 10 mmHg.s (P < 0.05); LD control: 387 +/- 167 vs. post L-NAME: 1737 +/- 617 mmHg.s (P < 0.05)). This effect was specific to activation of SFO efferents as the blood pressure responses to either, stimulation of PVN, or systemic administration of vasopressin were not potentiated by administration of L-NAME. These findings suggest that NO may be acting within PVN to inhibit further release of ANG, thereby attenuating the cardiovascular response to stimulation of SFO.
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PMID:Angiotensin II neurotransmitter actions in paraventricular nucleus are potentiated by a nitric oxide synthase inhibitor. 751 40

Magnocellular hypothalamic neurons of the paraventricular (PVN) and supraoptic (SON) nuclei have been shown to contain a wide variety of messenger molecules in addition to vasopressin and oxytocin, including the nitric oxide (NO)-synthesizing enzyme (NOS). In this paper we have investigated the effects of salt loading on the expression of NOS by means of immunohistochemistry and in-situ hybridization. The results show an increase in the number of NOS-immunoreactive (IR) neurons both in the PVN and the SON after 5 and 14 days of salt loading. Several of these neurons were double labelled with vasopressin antiserum. In situ hybridization showed a marked increase in the number of neurons expressing NOS mRNA and a stronger signal in individual neurons. The present results suggest a role for NO in the magnocellular hypothalamic system after salt loading.
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PMID:Nitric oxide synthase increases in hypothalamic magnocellular neurons after salt loading in the rat. An immunohistochemical and in situ hybridization study. 751 26

Rat aortic smooth muscle cells produced large quantities of nitric oxide (NO) after exposure to interleukin-1 beta, and this was depressed in the presence of the protein kinase C inhibitor bisindolylmaleimide. Intracellular cAMP levels were elevated mildly in cytokine-treated smooth muscle cells, and the presence of forskolin enhanced both the cAMP levels and NO production. Inhibition of GTP:cyclohydrolase I by 2,4-diamino-6-hydroxypyrimidine attenuated NO production by interleukin-1 beta-treated cells. GTP:cyclohydrolase is the regulatory enzyme for de novo tetrahydrobiopterin synthesis, and the latter is a required cofactor for NO synthase activity. Treatment of smooth muscle cells with forskolin induced GTP:cyclohydrolase mRNA expression, and simultaneous treatment of cells with forskolin and phorbol esters elicited NO production. Angiotensin II and arginine-vasopressin, acknowledged agonists for protein kinase C, elicited production of NO by forskolin-treated smooth muscle cells. These observations confirm the importance of GTP:cyclohydrolase activity for NO production by cultured smooth muscle cells and implicate both adenylyl cyclase and protein kinase C in this process.
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PMID:Simultaneous activation of adenylyl cyclase and protein kinase C induces production of nitric oxide by vascular smooth muscle cells. 752 13

The localisation and colocalisation of neuronal isoform (type I) nitric oxide synthase, endothelin-1, arginine-vasopressin and substance P in endothelial cells of rat coronary and femoral arteries was investigated by pre-embedding and postembedding immunocytochemistry. Nitric oxide synthase appeared in a high proportion of endothelial cells of both arteries (about 89% in the femoral artery, examined with the preembedding avidin-biotin-peroxidase method, and in almost all cells of the coronary artery, examined with the postembedding immunogold technique). Double immunogold labelling in single cells demonstrated the colocalisation of nitric oxide synthase with endothelin-1, arginine-vasopressin and substance P. The immunolabelling was mostly confined to the cytoplasmic matrix. It is suggested that nitric oxide synthase/nitric oxide and the peptides examined may be involved in local control of blood flow in coronary and femoral arteries.
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PMID:Localisation of nitric oxide synthase and its colocalisation with vasoactive peptides in coronary and femoral arteries. An electron microscope study. 752 54

I.c.v. administration of a nitric oxide (NO) synthase inhibitor (NG-monomethyl-L-arginine, NMMA, 500 micrograms/5 microliters) to conscious rats deprived of water for 24 h attenuated drinking and decreased glucose utilization in the subfornical organ and median preoptic nucleus. NMMA did not alter the enhanced glucose utilization in the hypothalamo-neurohypophysial system (HNS) of dehydrated rats, although it has been shown to increase, selectively, oxytocin (OT) secretion [18]. This suggests that NO may act in the neural lobe to inhibit OT secretion and promote the preferential release of vasopressin during dehydration. This effect is similar to the blockade of endogenous opiate receptors by naloxone.
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PMID:Central inhibition of nitric oxide synthase attenuates water intake but does not alter enhanced glucose utilization in the hypothalamo-neurohypophysial system of dehydrated rats. 752 94


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