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)

ANP receptor binding and desensitization were demonstrated in the A10 vascular smooth muscle cell (VSMC) line. Concomitantly, the ANP receptor coupled guanylate cyclase activity was reduced by the receptor down-regulation with ANP. The ANP stimulated cGMP accumulation is modulated by arginine-vasopressin, while the arginine-vasopressin mediated cAMP system remained unaffected by ANP. Results suggest negative coupling of arginine-vasopressin receptors to the guanylate cyclase activity, and indicate that the vasorelaxant activity of ANP might be regulated in part by arginine-vasopressin via specific receptor sites.
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PMID:Modulation of ANP receptor-mediated cGMP accumulation by atrial natriuretic peptides and vasopressin in A10 vascular smooth muscle cells. 289 30

Twenty-five years after the discoveries of the existence of atrial granules and of volume receptors in the heart atria the search for natriuretic hormones has led to the isolation and identification of the atrial natriuretic factors (ANF) now considered as a hormonal system. These peptides are probably synthesized and stored in the Golgi apparatus of cardiac myocytes and are released in response to atrial wall stretch following acute plasma volume expansion and increased central blood volume, e.g., during head-out water immersion, in arterial hypertension, or increased left and/or right atrial pressure in cardiac failure, but also possibly in response to increased frequency of myocardial contractions, e.g. in paroxysmal tachycardia. The mechanisms of the renal action of these potent natriuretic hormones are not yet precisely known. Increased GFR may contribute to the initial rise in urinary sodium excretion and increased renal medullary blood flow to the later phase of natriuresis. The proximal tubule, the thin descending and the ascending limb of Henle's loop and especially the medullary collecting tubule were so far incriminated as tubular sites of action of ANF. Finally, recycling of sodium in medullary tissue and secretion of sodium via back-flux from the interstitium into the medullary collecting tubule are postulated to result in the hypernatric urine observed after ANF administration. Direct suppression of the secretion of renin, aldosterone, vasopressin, and vasopressin-stimulated cAMP synthesis may also contribute to its diuretic, natriuretic, and antihypertensive effects. The renal hemodynamic and tubular as well as the adrenal and systemic vascular effects are related to enhanced cGMP synthesis in medium-sized arterial vessels, in glomeruli and specific tubular segments, and in adrenal tissue, and may be calcium dependent. Specific ANF-binding sites were detected in these target organs. Although increased ANF release was observed in response to atrial distension in various disease states, which may contribute to renal sodium elimination in human hypertension and congestive heart failure, further studies are needed to identify its precise physiological and pathophysiological significance.
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PMID:Atrial natriuretic hormones--thirty years after the discovery of atrial volume receptors. 294 41

This study examined the effects of transmural nerve stimulation, acetylcholine, adrenoceptor agonists and several peptides on the contractility of strips of human gallbladder in vitro. Acetylcholine caused concentration-related contractions of the tissues and the sensitivity to acetylcholine was similar in gallbladders with mild and severe chronic cholecystitis. Noradrenaline and adrenaline relaxed gallbladder strips, probably via beta 2-adrenoceptor stimulation. Transmural nerve stimulation always caused contractions, but in the presence of atropine inhibitory responses were demonstrable and these were antagonized by propranolol. There was no evidence of non-adrenergic inhibitory neural responses. Of the peptides tested, only cholecystokinin octapeptide (CCK-OP), gastrin, pentagastrin, substance P and caerulein caused contractions. Responses to CCK-OP, gastrin and pentagastrin were antagonized by dibutyryl cyclic GMP. Hormones which had no effect upon human gallbladder strips included motilin, secretin, bombesin, neurotensin, glucagon, vasopressin, VIP and somatostatin. Considerable differences therefore exist between human tissues and those from experimental animals with respect to the direct actions of neural and hormonal stimuli on gallbladder contractility.
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PMID:Contractility of human gallbladder muscle in vitro. 297 88

A survey of the literature reporting the in vivo biological activity of atrial natriuretic factor (ANF) is presented. Both the atrial extracts, in which ANF was first identified, and the peptides which have more recently been synthesized, have been shown to possess diuretic and saluretic properties. In addition, ANF decreased blood pressure and affected levels of aldosterone, renin, vasopressin and guanosine 3',5'-cyclic monophosphate (cGMP). The available evidence concerning likely mechanisms of action of ANF are presented and a pivotal role of ANF is suggested for blood pressure and volume regulation.
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PMID:Renal and systemic effects of atrial natriuretic factor. 299 Jul 75

Clonidine produced an increase of cGMP content and a decrease of the endogenous type II inhibitor of protein kinase in rat hypothalamic slices. When administered to rats, the effect of clonidine on type II inhibitor activity in the hypothalamus and brain-stem depended on the dose. Low doses (10-50 micrograms X kg-1 i.p.) produced an increase, probably by stimulating presynaptic alpha 2-adrenoceptors, whereas large doses (200-1000 micrograms X kg-1 i.p.) produced a decrease of type II inhibitor activity by stimulating postsynaptic receptors. The development of vasopressin hypertension was associated with a gradual reduction of the response of the type II inhibitor to low and high doses of clonidine. In vasopressin-hypertensive rats neither small nor large doses of clonidine were able to induce changes in type II inhibitor activity suggesting subsensitivity of pre- and postsynaptic alpha 2-adrenoceptors. However, clonidine appeared to be equally effective in blocking electrically stimulated [3H]noradrenaline release from hypothalamic slices of vasopressin-hypertensive and control, normotensive rats. Reduced reactivity of postsynaptic alpha 2-adrenoceptors seems to be of great importance since treatment of vasopressin-hypertensive rats with 6-hydroxydopamine resulted in a decrease of blood pressure and reappearance of the sensitivity of postsynaptic alpha 2-adrenoceptors to clonidine.
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PMID:Changed sensitivity of alpha 2-adrenoceptors mediating a decrease in protein kinase inhibitor activity in the brain of vasopressin-hypertensive rats. 300 71

Administration of clonidine produced biphasic changes in the type II inhibitor activity (endogenous inhibitor of protein kinases which specifically regulates phosphorylation mediated by cGMP-dependent system). Small doses of clonidine (10-50 micrograms/kg) produced an increase while large doses (200-1000 micrograms/kg) induced a decrease in the type II inhibitor activity. The both actions of clonidine were greatly reduced in vasopressin hypertensive rats suggesting subsensitivity of alpha 2-adrenergic receptors. Subsensitivity of postsynaptic alpha 2-receptors was also observed in anterior hypothalamus in in vitro experiments. Incubation of anterior and posterior hypothalamic slices with clonidine resulted in concentration-dependent increase in cGMP content and a decrease in the type II inhibitor activity. The clonidine action in anterior hypothalamus of vasopressin-hypertensive rats was greatly reduced. In contrast, the clonidine action in posterior hypothalamus was the same in vasopressin-hypertensive as in the control rats.
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PMID:The responsiveness of alpha 2-adrenergic receptors in hypothalamus of vasopressin-hypertensive rats. 300 36

The vasodilator 8-bromo-guanosine 3':5'-monophosphate (8-bromo-cGMP) effectively counteracts vasopressin-induced coronary artery constriction in a supported perfused working rabbit heart. In this preparation, the coronary arteries remain in contact with the beating heart. The obtuse marginal artery and portions of the left anterior descending coronary artery were deprived of endothelium. Perfusion was carried out with Krebs-Henseleit solution, oxygenated with a disposable infant oxygenator. The internal diameter of large coronary arteries was determined by color arteriography (injection of patent blue dye and gated photography). The effect of vasopressin with and without the addition of 8-bromo-cGMP on cardiac performance (cardiac output, left ventricular systolic pressure, left ventricular end-diastolic pressure, maximal rate of rise in left ventricular pressure [dP/dtmax], mean aortic pressure) and large coronary vessel and total coronary vascular resistance was determined in nine experiments. In addition, changes in coronary sinus partial pressure of carbon dioxide (PCO2) and pH were observed. Vasopressin alone caused a significant decline in coronary flow, myocardial oxygen consumption and coronary sinus pH. Cardiac performance declined, probably because of myocardial ischemia. Large coronary vessel and total coronary vascular resistance rose. The vasodilator 8-bromo-cGMP strongly inhibited the vasoconstrictor action of vasopressin, counteracted the increase in large and total coronary vascular resistance, prevented the fall in myocardial oxygen consumption and eliminated changes in pH or PCO2 of coronary sinus effluent. Because of the elimination of myocardial ischemia by 8-bromo-cGMP, cardiac performance was normalized.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of 8-bromo-cyclic guanosine monophosphate (cGMP) on coronary artery constriction in isolated rabbit hearts. 301 62

Angiotensin II, a potent vasoconstrictor peptide, increases free cytoplasmic Ca2+ concentration ([Ca2+]i) in vascular smooth muscle cells (VSMC) by release of nonmitochondrial Ca2+ stores and stimulates an amiloride-sensitive Na+ influx, presumably via Na+/H+ exchange. We recently have found that the angiotensin II-mediated change in VSMC intracellular pH has two components, an early rapid acidification phase and a slower recovery phase involving Na+-dependent alkalinization. In the present study, we show that the early acidification is not mediated via Na+/H+ exchange. Instead, we propose a mechanism which involves increases in [Ca2+]i and Ca2+ efflux with a subsequent rise in intracellular H+. Agonists, in addition to angiotensin II, which increase [Ca2+]i in cultured VSMC, including platelet-derived growth factor, vasopressin, and bradykinin, induce an acidification, while agonists which fail to raise [Ca2+]i do not. The time course and magnitude of agonist-stimulated 45Ca2+ efflux correlate with the acidification response. The angiotensin II concentration-response relationship for acidification and Ca2+ mobilization are similar. Furthermore, inhibition of changes in [Ca2+]i by treatment with phorbol ester, cyclic GMP, or quin2 loading prevent agonist-mediated acidification. The effects of altering extracellular [Ca2+] and [H+] on agonist-mediated intracellular acidification and H+ efflux suggest that the acidification is due to ATP-dependent unidirectional H+ influx, perhaps via the plasma membrane Ca2+-ATPase, and not to a Ca2+/H+ antiport. This agonist-mediated acidification represents a previously undescribed ionic event in VSMC activation which may be involved in excitation-response coupling.
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PMID:Early agonist-mediated ionic events in cultured vascular smooth muscle cells. Calcium mobilization is associated with intracellular acidification. 303 Oct 38

Sustained oscillations in extracellular free Ca2+ were shown to occur on addition of vasopressin, phenylephrine or angiotensin II in isolated rat liver perfused with low (10 microM)-Ca2+ medium. The amplitude and frequency of oscillation depend on hormone concentration. In contrast, Ca2+ releases on addition of ATP, t-butyl hydroperoxide or arachidonate do not exhibit oscillatory behaviour. The vasopressin-induced oscillations were suppressed by glucagon and dibutyryl 3',5'-cyclic AMP, but not by dibutyryl 3',5'-cyclic GMP. These observations in the extracellular space complement observations by Woods, Cuthbertson & Cobbold [(1986) Nature (London) 319, 600-602] on oscillations in intracellular free Ca2+ in single liver cells.
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PMID:Sustained oscillations in extracellular calcium concentrations upon hormonal stimulation of perfused rat liver. 303 78

Endothelial cells of the arterial wall can generate vasodilator and vasoconstrictor substances. The prototype of a vasodilator substance formed primarily in the endothelium is prostacyclin, although its main target under physiological conditions are the platelets. In addition, the endothelial cells respond to a variety of neurohumoral mediators by the liberation of an unidentified substance(s) (endothelium-derived relaxing factor) with a potent inhibitory effect on vascular smooth muscle, presumably because it accelerates the production of cyclic GMP in the latter. Endothelium-derived relaxing factor is very unstable, and has an extremely short half-life. It is inactivated by plasma proteins and thus does not fulfill a hormonal role. A metabolite of arachidonic acid may be involved in the production of endothelium-derived relaxing factor. Among the neurohumoral mediators which release it are: acetylcholine (through activation of muscarinic receptors), adenosine di- and triphosphate (P2-purinergic receptors), bradykinin, histamine (H1- or H2-histaminergic receptors, depending on the species), serotonin (S1-serotonergic receptors), substance P, oxytocin, thrombin and vasopressin (V1-vasopressinergic receptors). The release of the factor can also be triggered by aggregating platelets (because they release adenine nucleotides and serotonin) and by increases in shear stress. It is likely that endothelium-dependent dilatation helps to prevent intraluminal coagulation in arteries with a normal intima. Absence, or dysfunction of the endothelium may favor the occurrence of vasospasm. Endothelium-dependent relaxations are reduced in atherosclerotic blood vessels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The endothelium and arterial reactivity]. 349 May 30


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