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)

Exposure of human platelets to 10 discharges from a 4.5 microF capacitor charged at 3 kV permitted isolation of a stable preparation of permeabilized platelets that, after equilibration with Ca2+ buffers (pCa less than 6) for 15 min at O degrees C, secreted 5-hydroxytryptamine (5-HT) at 25 degrees C. Thrombin enhanced the sensitivity to Ca2+ of the secretion of 5-HT by about 10-fold, whereas Arg -vasopressin and the prostaglandin endoperoxide analogue, U-46619, increased sensitivity to Ca2+ by 3 to 4-fold. This action of thrombin was associated with stimulation of diacylglycerol formation, a marked increase in phosphorylation of protein P47 and a smaller increase in phosphorylation of the P-light chain of myosin. Thrombin exerted these effects at a [Ca2+ free] of 0.1 microM, suggesting that the receptor-activated breakdown of platelet phosphoinositides to diacylglycerol may not require prior Ca2+ mobilization in intact platelets. In both the presence and absence of thrombin, a higher [Ca2+ free] was required for optimal secretion than for maximal phosphorylation of P47 and myosin light-chain, indicating that Ca2+ and possibly diacylglycerol have roles in the secretory mechanism additional to activation of the enzymes that phosphorylate these proteins. Stable GTP analogues such as guanosine-5'-O-(3-thiotriphosphate) (GTP gamma S), and to a lesser extent GTP itself, enhanced the Ca2+ sensitivity of the secretion of 5-HT from permeabilized platelets. Moreover, GTP potentiated the stimulatory action of thrombin. These effects of GTP gamma S and GTP were associated with increased diacylglycerol formation and were inhibited by guanosine-5'-O-(2-thiodiphosphate) (GDP beta S) suggesting that a GTP-binding protein may play a role in the receptor-activated breakdown of phosphoinositides. However, as GDP beta S did not inhibit the potentiation of secretion caused by thrombin alone, a GTP-independent pathway of platelet activation may also exist.
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PMID:Receptor-induced diacylglycerol formation in permeabilized platelets; possible role for a GTP-binding protein. 609 73

Isolated urethral preparations from rabbit and man responded to transmural electrical stimulation with contraction when the basal tension was low, and with relaxation when the preparations were contracted by noradrenaline, clonidine, 5-hydroxytryptamine and lysine vasopressin. Both contractant and relaxant responses were abolished by tetrodotoxin, suggesting that they were caused by the action of transmitters released from nerves. The electrically induced contractions in the rabbit urethra had a threshold frequency of 5 to 6 Hz and maximum was reached at 40 Hz. The responses were markedly reduced by alpha-receptor blockers suggesting that the released contraction-mediating transmitter was mainly noradrenaline. The relaxant response was immediate and rapidly reversible. It was obtained at a threshold frequency of 1 to 2 Hz and maximum was reached at 10 to 15 Hz. It was not inhibited by propranolol, indomethacin, atropine or peptides such as substance P, VIP, vasopressin or somatostatin. Prostaglandin E2, isoprenaline, adenosine-5'-triphosphate and VIP relaxed the noradrenaline contracted rabbit urethra with a time course different from that of the electrically induced relaxation. Nifedipine and "calcium free" solution decreased the noradrenaline induced contraction but did not influence the relaxant response to electrical stimulation. It is suggested that the relaxant response of the isolated noradrenaline-contracted urethra to electrical stimulation is caused by an unknown transmitter released from nerves.
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PMID:Electrically induced relaxation of the noradrenaline contracted isolated urethra from rabbit and man. 613 Nov 47

781094 (2-(2(1, 4-benzodioxanyl))-2-imidazoline hydrochloride) is a potent competitive inhibitor of the aggregatory responses of human platelets induced by adrenaline (pA2 = 7.3) and UK-14304. 781094 is a more potent inhibitor of the pro-aggregatory response to clonidine than of that to methoxamine. The alpha 2/alpha 1-adrenoceptor selectivity ratio is 11.4. 781094 is a potent inhibitor of the binding of [3H]-dihydroergocryptine to platelet lysates. 781094 has no effect on the aggregatory responses of human platelets induced by adenosine-5'-pyrophosphate (ADP), 5-hydroxytryptamine, thrombin, U-46619, or arginine-vasopressin provided that the platelet-rich plasma does not exhibit enhanced responsiveness. In some instances high concentrations of 781094 potentiate the aggregatory response to collagen. In platelet-rich plasma which exhibits enhanced responsiveness, 781094 causes partial inhibition of the aggregatory responses to 5-hydroxytryptamine, ADP and vasopressin at concentrations similar to those required to inhibit the response to adrenaline. 781094 acts as a specific antagonist for the responses mediated by human platelet alpha-adrenoceptors and exhibits moderate selectivity for the alpha 2-adrenoceptors on this cell.
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PMID:Effect of 781094, a new selective alpha-adrenoceptor antagonist, on the aggregatory responses of human blood platelets and on binding of [3H]-dihydroergocryptine to these cells. 614 40

The distribution of vasopressin-, vasoactive intestinal polypeptide-, somatostatin-, avian pancreatic polypeptide-, 5-hydroxytryptamine- and glutamic acid decarboxylase-like immunoreactivity was analyzed in the suprachiasmatic nuclei of male and female golden hamsters. Vasopressin. Vasopressin-like immunoreactivity is localized within neurons, dendrites and axons throughout the rostrocaudal extent of the suprachiasmatic nuclei. Immunoreactive perikarya are restricted to the dorsomedial aspect of each nucleus and occur in highest numbers within the intermediate two-thirds of the rostrocaudal axis. Axons containing vasopressin-like immunoreactivity form a dense plexus in the dorsomedial suprachiasmatic nuclei and in a vertical column at the lateral aspect of each nucleus. Somatostatin. Somatostatin-like immunoreactivity is also contained in neurons in the dorsomedial aspect of the suprachiasmatic nuclei and in thin varicose axons distributed throughout the suprachiasmatic nuclei in a pattern similar to that of vasopressin-immunoreactive axons. Vasoactive intestinal polypeptide. Vasoactive intestinal polypeptide-immunoreactive neurons are concentrated in the ventrolateral portion of each nucleus and occur almost exclusively within the intermediate two-thirds of the rostrocaudal axis. An extremely dense plexus of varicose axons exhibiting vasoactive intestinal polypeptide-like immunoreactivity extends throughout the suprachiasmatic nuclei and passes out of the dorsal aspect of each nucleus into the periventricular and anterior hypothalamic areas. Avian pancreatic polypeptide. Avian pancreatic polypeptide-like immunoreactivity is restricted to axons which arborize within the ventrolateral aspect of each nucleus. These fibers extend throughout the rostrocaudal extent of each nucleus and partially overlap the terminal field of retinal afferents. Glutamic acid decarboxylase. A very dense plexus of axonal varicosities exhibiting glutamic acid decarboxylase-like immunoreactivity fills both the dorsomedial and ventrolateral portions of the suprachiasmatic nuclei throughout the rostrocaudal extent of each nucleus. Lightly stained immunoreactive perikarya also occur throughout the suprachiasmatic nuclei. 5-Hydroxytryptamine. 5-Hydroxytryptamine-like immunoreactivity is restricted to axons which form a plexus in the ventromedial portion of each nucleus that is most dense in the intermediate two-thirds of the rostrocaudal axis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The suprachiasmatic nucleus of the golden hamster: immunohistochemical analysis of cell and fiber distribution. 615 Nov 47

We have assessed the influence of acute bilateral nephrectomy, of captopril and saralasin, on the hypotensive activity of neurotensin (NT) and of various hypotensive drugs in pentobarbital-anesthetized rats. The results show that the hypotensive activity of NT and of compound 48/80 (C48/80), in contrast to that of histamine, of 5-hydroxytryptamine and of hexamethonium, is markedly reduced, especially for NT, in nephrectomized as compared to sham operated rats. The pretreatment of rats with captopril (10 mg kg-1, i.v.) or with saralasin (20 micrograms kg-1 min-1, i.v.) was found to inhibit significantly the hypotensive activity of NT and of C48/80. Adrenalectomy restored partially the hypotensive activity of NT in nephrectomized rats. The potent vasopressin antagonist [d(CH2)5 Tyr(Me)AVP] did not alter the refractoriness of nephrectomized rats to the hypotensive activity of NT. Neither nephrectomy nor saralasin were found to interfere with the ability of NT or of C48/80 to evoke an increase of plasma histamine level or of the hematocrit. The results were interpreted as an indication that NT produces part of its hypotensive effect in anesthetized rats by reducing the activity of the renin angiotensin system. The results also suggest that part of the refractoriness of nephrectomized rats to the hypotensive activity of NT could be due to the release of catecholamines from adrenal glands by NT. Endogenous vasopressin does not appear to contribute to the refractoriness of nephrectomized rats to the hypotensive action of NT.
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PMID:Partial blockade of neurotensin-induced hypotension in rats by nephrectomy captopril and saralasin. Possible mechanisms. 619 Dec 40

Five undeca- and six C-terminal heptapeptide substance P (SP) analogues were tested for their capacity to block the contractile effect of SP on the guinea-pig isolated taenia coli. They had one feature in common, namely substitutions in positions 7 and 9 in the SP molecule. In the majority of analogues D-tryptophan was used for these substitutions. All analogues tested were found to be competitive antagonists to exogenous SP and to be capable of blocking the electrically induced non-cholinergic, non-adrenergic neuronal contraction of the taenia. Of the undecapeptides, (D-Arg1, D-Pro2, D-Trp7,9, Leu11) SP and (D-Arg1, D-Trp7,9, Leu11) SP (Spantide) had the highest pA2 value, 7.1-7.2, and the lowest IC50 value, 10(-6) M. The pA2 values of the heptapeptides were generally lower. Three of the most potent antagonists were tested for specificity and found to block the smooth muscle contraction induced by SP, physalaemin, eledoisin and bombesin but not that induced by bradykinin, carbachol, 5-hydroxytryptamine, histamine, prostaglandins and vasopressin. The SP antagonists were also tested for spasmogenic effect on the taenia and for their capacity to release histamine from rat isolated peritoneal mast cells. The spasmogenic activity displayed by most of the SP antagonists tested is likely to be related to their ability to release histamine since the contractile response was reduced by mepyramine, a histamine H1-receptor antagonist. (D-Arg1, D-Trp7,9, Leu11) SP was notable for combining a high antagonistic potency with a weak spasmogenic effect (and poor histamine releasing effect).
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PMID:Biological evaluation of substance P antagonists. 620 86

In vitro studies were undertaken to determine the reactivity and contractility of the rat main pulmonary artery (RPA) to some selected vasoactive agents. Oxytocin was found to be inactive RPA exhibited a poor responsiveness to vasopressin, acetylcholine, histamine, and bradykinin. Prostaglandins B2 and E2, K+, angiotensin, sympathomimetic agents (epinephrine and isoproterenol), 5-hydroxytryptamine (5-HT), and [Ca2+]0 were found to produce, consistently, potent and concentration-related contractions of the RPA. Pulmonary arterial strips that were precontracted with 5-HT responded with relaxations to isoproterenol in low concentrations and with contractions in high concentrations. Blockade of isoproterenol-induced relaxation by propranolol provides evidence for the existence of specific beta-adrenoceptors in RPA. The selective antagonism of contractile responses induced by epinephrine, 5-HT, acetylcholine, and histamine by phentolamine, methysergide, atropine, and pyrilamine, respectively, provides evidence for the occurrence of specific alpha-adrenergic, "D"-serotonin as well as some cholinergic (muscarinic) and H1-histamine receptors in the RPA.
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PMID:Reactivity and contractility of rat main pulmonary artery to vasoactive agents. 625 36

Cyclic AMP and Ca2+ are intracellular mediators of hormone action. Catecholamines interact with beta adrenoceptors to activate adenylate cyclase or with alpha 2 adrenoceptors to inhibit adenylate cyclase. Alpha 1 adrenoceptor activation results in elevation of cytosol Ca2+ and an increased breakdown of phosphatidylinositol. In blowfly salivary glands, 5-hydroxytryptamine (5-HT) interacts with beta type receptors resulting in adenylate cyclase activation while alpha type receptors are involved in phosphatidylinositol breakdown and elevation of cytosol Ca2+. The link between Ca2+ mobilization and phosphatidylinositol breakdown remains to be established but breakdown of the receptor-regulated pool of phosphatidylinositol is not secondary to the rise in Ca2+. Direct addition of 5-HT to cell-free homogenates of blowfly salivary glands results in activation of phosphatidylinositol breakdown in the absence of Ca2+. In rat liver plasma membrane preparations, vasopressin increases phosphatidylinositol breakdown in the absence of Ca2+ or cytosol if deoxycholate is present. The data do not indicate whether hormone activation increases the availability of substrate to enzymatic hydrolysis or activates phospholipase C. However, they demonstrate that hormones directly accelerate phosphatidylinositol breakdown.
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PMID:Hormonal regulation of phosphatidylinositol breakdown. 630 22

All cell-surface receptors that bring about a rise in cytosol Ca2+ concentration upon stimulation appear also to provoke enhanced metabolism of inositol phospholipids. For many years, it has been thought that the initiating reaction in this response is phosphodiesterase-catalysed breakdown of phosphatidylinositol (PtdIns). However, recent experiments with hepatocytes, parotid gland and blowfly salivary gland have demonstrated very rapid breakdown of phosphatidylinositol-4, 5-bisphosphate (PtdIns4,5P2), and maybe also of PtdIns4P, in cells stimulated by Ca2+-mobilizing stimuli (V1-vasopressin, angiotensin, alpha 1-adrenergic, muscarinic cholinergic, substance P and 5-hydroxytryptamine). As with the disappearance of PtdIns that had been studied previously, this response is not Ca2+-mediated and shows a receptor occupation dose-response curve. The PtdIns 'breakdown' studied previously was probably utilization of PtdIns for resynthesis of polyphosphoinositides to replace the degraded PtdIns4,5P2. We suggest that the primary event in receptor-stimulated inositol phospholipid metabolism is phosphodiesterase attack upon PtdIns4,5P2 to yield 1,2-diacylglycerol and inositol-1,4, 5-trisphosphate, and that this is an essential coupling event in a general mechanism by which receptors mobilize Ca2+ in the cytosol of stimulated cells.
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PMID:Polyphosphoinositide breakdown as the initiating reaction in receptor-stimulated inositol phospholipid metabolism. 630 23

The effects of vasopressin on the cerebral circulation were studied in conscious goats and in isolated human and goat cerebral arteries. Infusion of 1 to 12 mU of vasopressin into the internal maxillary artery of unanesthetized goats caused dose-dependent reductions in cerebral blood flow, a decrease of 36 +/- 4.7% (mean +/- S.E.) occurring with the highest dose. Cumulative application of vasopressin (10(-12) to 10(-6) M) markedly constricted human and goat cerebral arteries in vitro, the effect being more prominent in human vessels. (1-Deaminopenicillamine, 4-valine)-8-D-arginine-vasopressin, a competitive antagonist of the pressor effects of vasopressin, partially inhibited the cerebral vasoconstriction produced by vasopressin in vivo and in vitro without affecting the vasoconstrictor responses to norepinephrine, 5-hydroxytryptamine and potassium chloride. The results indicate that low concentrations of vasopressin produce constriction of cerebral vessels by direct excitatory effects on specific receptor sites. This effect should be considered in certain pathophysiological states in which vasopressin is released in amounts that could interfere with the proper blood supply to the brain.
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PMID:Evidence for the direct effect of vasopressin on human and goat cerebral arteries. 670 22


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