Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High-affinity binding sites for endothelin have been found in a human placenta membrane preparation. 125I-endothelin bound to placenta membranes at 20 degrees C with an association half-time of 30 min, whereas the binding was only slowly reversed with a dissociation half-time of 250 min. In saturation experiments, a single class of high-affinity binding sites was identified with an apparent dissociation constant (KD) of 24 pM and a maximal density of 240 fmol per mg of protein. The binding of 125I-endothelin was half-maximally inhibited by cold endothelin at a concentration (IC50) of 140 pM. In contrast, no inhibition was found at 10(-4) M for a variety of vasoactive peptides such as angiotensin II, vasopressin, neuropeptide Y, substance P, CGRP, bradykinin, leucine enkephalin or dynorphin A. Similarly, the binding was modulated neither by the calcium channel blockers nifedipine, verapamil or diltiazem, nor by the calcium channel agonist Bay k 8644. There was also no effect with the structurally-related bee venom apamin. Using this membrane preparation, endothelin-like activity could be measured in the medium of cultured human endothelial cells by competition binding technique.
 ...
PMID:Specific receptors for endothelin on membranes from human placenta. Characterization and use in a binding assay. 254 8

The effects of Ca2+, ionophore A23187, and vasopressin on CTP:phosphocholine cytidylyltransferase were investigated. Cytidylyltransferase is present in the cytosol and in a membrane-bound form on the microsomes. Digitonin treatment caused release of the cytosolic form rapidly. Addition of 7 mM Ca2+ to hepatocyte medium resulted in a 3-fold decrease in cytidylyltransferase released by digitonin treatment (1.7 +/- 0.1 nmol/min per mg compared to 5.1 +/- 0.2 nmol/min per mg in the control). Verapamil, a calcium channel blocker, partially overcame this effect of Ca2+. Ionophore A23187 and vasopressin both mimicked the effect of Ca2+ and resulted in a decrease in cytidylyltransferase release (2.4 +/- 0.1 nmol/min per mg and 2.5 +/- 0.2 nmol/min per mg, respectively) compared to control (3.4 +/- 0.1 nmol/min per mg). In agreement with the digitonin experiments, incubation with 7 mM Ca2+ resulted in a decrease in cytidylyltransferase in the cytosol (from 4.0 to 1.2 mol/min per mg) and a corresponding increase in the microsomes (from 0.6 to 2.4 nmol/min per mg). Verapamil partially blocked this translocation caused by Ca2+. Ionophore A23187 and vasopressin also caused translocation of the cytidylyltransferase from the cytosol to the microsomes. The addition of Ca2+ also resulted in an increase in PC synthesis. With 7 mM Ca2+ in the medium, the label associated with PC increased to 3.8 +/- 0.1.10(6) dpm/dish from 2.7 +/- 0.1.10(6) dpm/dish after 10 min. PC degradation was also affected, since 7 mM Ca2+ in the medium resulted in an increase in LPC formation both in the cell and the medium. We conclude that high concentrations of calcium in the hepatocyte medium can cause a stimulation of CTP:phosphocholine cytidylyltransferase and PC synthesis in cultured hepatocytes.
 ...
PMID:Stimulation of CTP: phosphocholine cytidylyltransferase and phosphatidylcholine synthesis by calcium in rat hepatocytes. 254 62

Endothelins are a group of potent vasoconstrictors whose structure was deduced from genomic DNA. ET-1 was first isolated from culture supernatants from porcine endothelial cells and ET-3 was identified from a rat DNA library. We report on the binding of 125I-ET-1 to zona glomerulosa cells in culture and on its ability to stimulate aldosterone secretion. Cultured calf adrenal zona glomerulosa cells have saturable, high affinity [Kd = 1.00 +/- 0.17 X 10(-10) M (SEM)] receptors which bind ET-1 in a temperature and time dependent manner. Binding was specific and angiotensin II, vasopressin, ANP, BNP, apamin, calcium channel agonists or antagonists did not interact with the receptor. ET-3 displaced 125I-ET-1 from the receptor with a relative potency of 0.39 +/- 0.1% (SEM) that of ET-1. ET-1 incubated with cultured glomerulosa cells stimulated aldosterone secretion in a dose dependent manner but it was less potent than angiotensin II. ET-3 had less than 1% the relative potency of ET-1 stimulating aldosterone secretion. This data suggest that ET-1 is an independent stimulator of aldosterone secretion and we are speculating that it might be important in those situations, like in malignant hypertension, where endothelial damage might result in increased ET-1 production.
 ...
PMID:Endothelin binding to cultured calf adrenal zona glomerulosa cells and stimulation of aldosterone secretion. 254 37

The synthesis of new radiolabelled compounds and the evolution of the techniques designed to study the hormonal receptors allow a better understanding of their properties. Three types of vasopressin receptors have been described: the V1a receptor of liver and blood vessels, the V1b receptor of hypophysis and the V2 receptor of kidney. Such a classification was based on two criteria: The structure of the binding site and the nature of the second messenger produced. The V2 receptor coupled positively to adenylate cyclase regulates the water reabsorption via the increase of intracellular cyclic AMP. The V1a and V1b receptors involved in glycogenolysis, contraction and probably neurotransmission mobilize intracellular calcium via a positive coupling to phospholipase C. These two receptors exhibit different recognition patterns for vasopressin analogues. In mammals, the oxytocin receptors are mainly involved in myometrial contraction and lactation. Their characterization are generally difficult since they also interact with vasopressin and are sometimes colocated with vasopressin receptors. As for V1 receptor, they are coupled to phospholipase C and mobilized intracellular calcium. The receptors of angiotensin II regulate the blood pressure by different mechanisms. They are coupled to at least two transduction mechanisms (positive coupling to phospholipase C and negative coupling to adenylate cyclase). Electrophysiological data seems to indicate that such receptor may also control a calcium channel. Yet different molecules (cAMP, calcium, inositol phosphates, diacyl-glycerol) trigger the hormonal effect of angiotensin II inside the cell.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Vasopressin, oxytocin and angiotensin receptors in mammals]. 269 9

1. A low concentration of serotonin (3 nmol/L), which did not exert a direct vasoconstrictor action, amplified the responses to certain other vasoconstrictor agents (alpha 1-adrenoceptor agonists, KCl, ATP and vasopressin) in isolated perfused segments of the rat tail artery. 2. Low concentrations of serotonin (0.3 and 1 nmol/L) amplified vasoconstrictor responses to sympathetic nerve stimulation, but higher concentrations of serotonin (10 and 30 nmol/L) produced vasoconstriction and reduced responses to sympathetic nerve stimulation. 3. The calcium channel blocking drug diltiazem (1 and 10 mumol/L) produced concentration-dependent reductions of vasoconstrictor responses to phenylephrine. The amplifying effect of serotonin on responses to phenylephrine was attenuated by 1 mumol/L and abolished by 10 mumol/L diltiazem, and was also abolished in a Ca2+-free medium. 4. Ketanserin (10 nmol/L) antagonized the vasoconstrictor action of serotonin and, to a lesser extent, the vasoconstrictor actions of phenylephrine and noradrenaline. It abolished the amplifying effect of a low concentration of serotonin on responses to noradrenaline and phenylephrine. 5. The amplification of vasoconstrictor response in the rat tail artery by serotonin appears to be due to activation of receptors of the 5-HT2 subtype which are coupled to an increase in Ca2+ influx into the vascular smooth muscle cells.
 ...
PMID:Amplification by serotonin of responses to other vasoconstrictor agents in the rat tail artery. 280 36

Previous investigations have shown that rat atrial natriuretic peptide (r-ANP,5-28, atriopeptin III), antagonizes the effects of various pressor hormones (angiotensin II, vasopressin and norepinephrine) but is ineffective against pressor responses to acute spinal cord stimulation. Because the latter are believed to be mediated by intrajunctional alpha-1 adrenoceptors, whereas the others are thought to involve mainly extrajunctional receptors, we explored the possible specificity of r-ANP for alpha adrenoceptor subtypes, by comparing r-ANP, the calcium channel blocker nifedipine and the vasodilator sodium nitroprusside in their ability to inhibit pressor responses to the alpha-2 and alpha-1 adrenoceptor agonists, clonidine and phenylephrine, in pithed, vagotomized rats. Acute pressor responses to bolus-injected clonidine were dose-dependently attenuated by both r-ANP (up to 21%) and nifedipine (up to 37%), but acute pressor responses to phenylephrine were unaffected. Sodium nitroprusside inhibited pressor responses to clonidine (up to 67%) and phenylephrine equally (up to 66%). Pressor responses during constant infusions of clonidine and phenylephrine were attenuated similarly by r-ANP and nifedipine. This pattern of results, alpha-2 adrenoceptor specificity during immediate pressor responses but not during sustained pressor responses, suggests that r-ANP, like nifedipine, attenuates those adrenoceptor-mediated pressor responses which depend on slow transmembrane calcium fluxes.
 ...
PMID:Differential inhibition of alpha adrenoceptor-mediated pressor responses by rat atrial natriuretic peptide in the pithed rat. 299 43

The vasoconstrictor effects of several hormonal systems, including catecholamines, the renin-angiotensin-aldosterone system and vasopressin, are mediated by calcium. Calcium channel inhibitors acting on smooth muscle therefore exert a potent vasodilator effect which can be of benefit for the treatment of human arterial hypertension. Single doses of nifedipine or verapamil induce a rapid and pronounced fall in blood pressure and can be used as emergency treatments of acute, severe hypertension. Blood pressure response to these drugs can be predicted from a variety of parameters, such as peripheral arterial resistance, age and activation of the renin-angiotensin system. The anti-hypertensive activity of calcium channel inhibitors is maintained in long-term treatments, whether they are administered alone or associated with one or two other drugs, as in hypertensions difficult to control. The advent of new compounds with long-lasting effects should encourage the development of this new category of anti-hypertensive agents.
 ...
PMID:[Treatment of human arterial hypertension. Role of calcium channel inhibitors]. 315 59

The effects of the calcium channel blocker verapamil on simultaneously recorded uterine and pressor responses to the equipotent (in eliciting these responses) oxytocin-vasopressin analogue, oxypressin, were studied in urethan-anesthetized and pentolinium- and indomethacin-treated rats during injections and infusions of this analogue. Doses of verapamil that almost completely blocked the pressor response to infused oxypressin had no effect on a pressor response to injected oxypressin of equal magnitude. Larger doses of verapamil blocked the pressor response to injected oxypressin somewhat. Uterine responses were only marginally affected by these doses of verapamil, and there was no significant difference between infusion and injection or between estrus and diestrus.
 ...
PMID:Verapamil blockade of pressor and uterine responses to AVP-OT analogue, oxypressin. 333 72

Human myometrial visceral and vascular preparations and placental chorionic and stem villous vessels were dissected from myometrial and placental specimens obtained at term Caesarean section and after vaginal delivery. Vascular ring preparations and myometrial strips were mounted in organ bath and isometric tension recorded. Only myometrial preparations developed spontaneous contractile activity, which was effectively blocked by the calcium channel blocker nitrendipine (NTD) 10(-7) M. Pretreatment with calcium-depleted medium for 30 min. almost abolished myometrial responses to high K+ (124 mmol), oxytocin (OX) and prostaglandin F2 alpha (PGF2 alpha). Vascular responses to high K+ (124 mmol) were also nearly abolished by such treatment. However, noradrenaline (NA), vasopressin (VP) and PGF2 alpha in myometrial arteries and PGF2 alpha in chorionic vessels and stem villous arteries induced significant, but reduced contractions after calcium depletion. In all vascular preparations, exposed to calcium-depleted medium, NTD (10(-8) M) almost abolished contractions induced by calcium (0.1-4.0 mM) in the presence of K+ (124 mmol) and depressed responses to calcium in the presence of the other agonists tested. NTD (10(-10)-10(-7) M) depressed myometrial contractions induced by K+, OX and PGF2 alpha more effective than vascular responses to K+, NA, VP and PGF2 alpha in the myometrial arteries and K+ and PGF2 alpha in the placental arteries. It is concluded that activation of contraction in vessels from the human utero-placental unit implies multiple cellular sources of calcium, while in myometrial smooth muscle, influx of superficially bound calcium may be an important initial step in contractile activation. Treatment with calcium channel blockers during late human pregnancy might involve relaxation of the myometrium together with vasodilatation of the myometrial and foetal placental vascular beds.
 ...
PMID:Inhibitory effects of nitrendipine on myometrial and vascular smooth muscle in human pregnant uterus and placenta. 346 59

Arginine-vasopressin (AVP) stimulates adrenocorticotropin and beta-endorphin release from corticotrophs of the anterior pituitary gland through mechanisms which are not initiated by an elevation of the cellular levels of adenosine-3',5'-cyclic-monophosphate. In the present study the effect of AVP on the cytoplasmic concentrations of free calcium ions in rat anterior pituitary cells was examined. Cytosolic free Ca2+ concentrations were monitored directly using the new, intracellularly trapped fluorescent indicator fura-2. In cells incubated in medium containing 1.3 mmol/l Ca2+, AVP (100 nmol/l) caused an immediate elevation of the cytoplasmic Ca2+ concentration by about 50 nmol/l (P less than 0.001). The intracellular Ca2+ levels remained elevated during the observation period of 2-3 min. This effect of AVP was blocked by a specific vasopressin antagonist. By contrast, the glucocorticoid dexamethasone did not affect the AVP-induced elevation of cytosolic Ca2+ concentration. When the cells were incubated in Ca2+-free medium (Ca2+ omitted, EGTA 2 mmol/l), the AVP-induced as well as the K+ depolarization-induced increase in free cytoplasmic Ca2+ were abolished, whereas the ionophore ionomycin evoked a rapid transient elevation of free Ca2+. The increase in cytoplasmic Ca2+ concentration induced by AVP was preserved in medium containing the calcium channel blockers Mg2+ (Mg2+ 31.2 mmol/l; Ca2+ 1.3 mmol/l) or nifedipine (1 mumol/l). The potassium-evoked calcium signal was blocked by Mg2+ (31.2 mmol/l). We conclude that vasopressin induces a rapid rise in the cytoplasmic concentration of free calcium ions in corticotrophs. Vasopressin may mobilize calcium through mechanisms that neither are glucocorticoid-sensitive nor involve the influx of extracellular calcium through voltage-dependent calcium channels.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Intracellular free calcium concentration in rat anterior pituitary cells as indicated by fura-2: effect of arginine-vasopressin. 368 98


<< Previous 1 2 3 4 5 6 7 Next >>