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)

Aggregation of human platelets by vasopressin is potently inhibited by 1-[beta mercapto-(beta, beta'-cyclopentamethylene propionic acid)]-L-arginine vasopressin, a selective vasopressor (V1) antagonist. 1-Desamino-8-D-arginine-vasopressin, a selective anti-diuretic (V2) agonist failed to induce aggregation and acted as a weak antagonist. Vasopressin analogues which lacked the N-terminal amino group or which contained an uncharged amino acid residue at position 8 acted as partial agonists for the human platelet. The response to such partial agonists could be enhanced by increasing the cytosolic Ca2+ concentration but not by altering the level of cyclic-3', 5'-AMP. These observations provide further evidence indicating that the platelet vasopressin receptor is of the V1 sub-type.
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PMID:Some properties of the human platelet vasopressin receptor. 632 Apr 89

Arginine vasopressin (AVP) and angiotensin II (ANG II) reduce the glomerular filtration rate and ultrafiltration coefficient. Vasodilatory prostaglandins (PG) antagonize these effects. AVP and ANG II also cause mesangial cell contraction. Therefore, possible PG stimulation by these peptides and two vasopressin analogues was studied in cultured rat glomerular mesangial cells. The effect of altered calcium availability on PG production was also studied. Glomeruli from 75-100-g Sprague-Dawley rats were cultured in supplemented nutrient media for 28 d and experiments were performed on the first passage. Mesangial cell morphology was confirmed by electron microscopy. Cells produced PGE2 much greater than PGF2 alpha greater than 6-keto-PGF1 alpha greater than thromboxane B2 when incubated with the divalent cation ionophore, A23187, or arachidonic acid (C20:4). ANG II and AVP selectively stimulated PGE2 at threshold concentrations of 10 nM ANG II and 100 pM of AVP. The effects of the antidiuretic analogue 1-desamino-8-D-arginine vasopressin (dDAVP) and the antipressor analogue [1-(beta-mercapto-beta beta-cyclopentamethylene propionic acid)-4-valine, 8-D-arginine]-vasopressin (d[CH2]5VDAVP), were studied. Neither compound stimulated PGE2 and preincubation with d(CH2)5VDAVP abolished, and dDAVP blunted, AVP-enhanced PGE2 production. Incubation in verapamil, nifedipine, or zero calcium media blocked peptide-stimulated PGE2 production. Increasing extracellular calcium or adding A23187 increased PGE2 synthesis. Selective stimulation of PGE2 by ANG II or AVP in mesangial cells suggests a hormone-sensitive phospholipase and a coupled cyclooxygenase capable of synthesizing only PGE2. Since neither vasopressin analogue stimulated PGE2, but both blocked AVP-enhanced PGE2 production, we conclude that these cells respond to the pressor activity of AVP. This is a calcium-dependent process. Selective stimulation of PGE2 by ANG II and AVP may modulate their contractile effects on the glomerulus.
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PMID:Prostaglandin synthesis by rat glomerular mesangial cells in culture. Effects of angiotensin II and arginine vasopressin. 640 23

The effects of naturally occurring lysine and arginine vasopressins (LVP and AVP) were compared with those of 1-deamino-8-D-arginine-vasopressin (dDAVP) and 1-deamino-4-valine-D-arginine-vasopressin (dVDAVP). The changes of minute diuresis, urinary osmolarity and the duration of action were followed. dDAVP and dVDAVP in a single intravenous and intranasal dose decreased the diuresis more markedly (3.5-fold) and for a longer duration (3.3-fold) than did LVP in patients with central diabetes insipidus. The administration of dDAVP and dVDAVP in the form of sublingual tablets also proved to be effective, where dVDAVP acted more markedly and longer (16 hrs) than dDAVP (12 hrs) in a single dose of 30 micrograms. During one week of sublingual dDAVP administration, the accumulation of the drug was indicated by the gradual decrease of diuresis and the increase of urine osmolarity. The misuse of such highly active drugs may even result in iatrogenic inappropriate ADH syndrome (Schwartz-Bartter). The danger of this syndrome will be demonstrated in a case history. Some more recently synthesized vasopressin analogues with antagonistic action on the diuresis may have an important role in the therapy of Schwartz-Bartter syndrome. The authors present their results with one of these antagonists [1-(beta-mercapto-beta, beta-cyclopentamethylene-propionic acid), 2-O-ethyltyrosine, 4-valine] arginine vasopressin (d/CH2/5Tyr/Et/VAVP) both in Brattleboro and in R-Amsterdam rats. This analogue blocks the antidiuretic effect of both exogenous and endogenous vasopressin.
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PMID:[The effect of vasopressin analogs on water metabolism]. 666 81

The effect of [1-(beta-mercapto-beta, beta- cyclopentamethylene -propionic acid),2-0- ethyltyrosine ,4-valine]-arginine vasopressin on the water metabolism was studied in rats. The compound decreases the antidiuretic action of exogenous vasopressin in Brattleboro rats; in rats without diabetes insipidus it causes temporary polyuria and eliminates the response of antidiuresis to an osmotic stimulus. The results indicate that this compound can block the antidiuretic action of both exogenous and endogenous vasopressin.
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PMID:Effect of the vasopressin antagonist d/CH2/5Tyr/Et/VAVP on the antidiuretic action of exogenous and endogenous vasopressin. 673 Aug 54

A rat model of the Schwartz-Bartter syndrome was created by the administration of a high dose of a long-acting vasopressin preparation (pitressin tannate ) together with a forced water intake. The treatment led to water retention, hypernatriuria , marked hyponatraemia (in 4-5 days) and severe cerebral oedema. These changes could be prevented by the simultaneous administration of [1-(beta-mercapto-beta, beta- cyclopentamethylene -propionic acid),2-0- ethyltyrosine ,4-valine]arginine vasopressin. The observations indicate that this vasopressin antagonist analogue might be of use in the future as an effective drug against the Schwartz-Bartter syndrome.
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PMID:Prevention of hyponatraemia and cerebral oedema by the vasopressin antagonist d/CH2/5Tyr/Et/VAVP in rats treated with pitressin tannate. 673 Aug 55

The effect of [1-(beta-mercapto-beta,beta- cyclopentamethylene -propionic acid)2-0- ethyltyrosine ,4-valine] arginine vasopressin on the water metabolism was studied in rat. The compound was found to be able to block the antidiuretic action of both exogenous and endogenous vasopressin. A rat model of the Schwartz-Bartter syndrome was created by the administration of a high dose of a posterior pituitary preparation (Pitressin tannate ) together with a forced water intake. The antagonist prevented water retention and averted the enhanced natriuresis and hyponatraemia, and cerebral oedema did not develop. The observations suggest that this vasopressin antagonist might be of use in the future as an effective drug against the Schwartz-Bartter syndrome.
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PMID:Effect of the vasopressin antagonist d(CH2)5 Tyr(Et)VAVP on diuresis in rat. 673 24

Antidromically identified paraventricular neurones were recorded simultaneously with intramammary pressure in urethane (1.2 g/kg) anaesthetized rats during suckling. The correlation of the firing pattern of these neurones with milk ejection enabled distinction between oxytocin and vasopressin neurones. Oxytocin neurones displayed a short (2-6 s) characteristic high-frequency burst of spikes. This activation probably occurred simultaneously in all oxytocin neurones 12-18 s before milk ejection and was regular in both frequency and amplitude (total number of spikes). The role of neurohypophysial peptides and analogues in the control of these characteristics was studied. Injecting 10 pg, 100 pg and 1 ng of oxytocin into the 3rd ventricle increased background activity of slow-firing oxytocin neurones (less than 3 spikes/s) and had a strong dose-dependent facilitatory effect on the milk ejection reflex, increasing both the amplitude and frequency of neurosecretory bursts. No effect was observed on non-neurosecretory neurones. Such injection also triggered the milk ejection reflex when it had not appeared an hour after suckling began. Oxytocin did not itself induce neurosecretory activation, which only appeared if the young rats were sucking. Injecting oxytocin into the lateral ventricle was less effective than into the 3rd ventricle. No effect was observed after injection into the venous blood or into the 4th ventricle, which suggested that oxytocin acts in the hypothalamus. Injecting mesotocin or isotocin into the 3rd ventricle had a facilitatory effect similar to that of oxytocin but vasopressin, vasotocin, MIF I (pro-leu-gly-NH2, terminal triplet oxytocin) or bovine neurophysins I and II did not modify neurosecretory activation or the milk ejection pattern. Injecting an oxytocin antagonist, ([1(beta-mercapto-beta, beta cyclopentamethylene propionic acid), 8-ornithine] vasotocin, d(CH2)5OVT) into the 3rd ventricle decreased milk ejection frequency and considerably delayed the reappearance of the first milk ejection. This resulted from a decrease in both frequency and amplitude of neurosecretory bursts, which were too small to induce detectable oxytocin release. Moreover, d(CH2)5OVT suppressed the facilitatory effect of exogenous oxytocin. Under normal conditions, endogenous oxytocin seemed to be involved in the control of neurosecretory activation. Injecting 1 ng oxytocin or 1 or 10 ng vasopressin into the 3rd ventricle did not modify the firing pattern of vasopressin neurones whether activated by hyperosmotic stimulation (1 ml NaCl, 9% solution (w/v) I.P.) or not.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Electrophysiological evidence for facilitatory control of oxytocin neurones by oxytocin during suckling in the rat. 674 98

We used a structural analogue of arginine vasopressin (AVP) and investigated the role of AVP in the maintenance of mean arterial pressure (AP) in anesthetized, water-deprived rats. The administration of [1(beta-mercapto-beta,beta-cyclopentamethylene propionic acid) 4-valine-8-D-arginine] vasopressin, d(CH2)5VDAVP, completely inhibited to 30-40 mma Hg rise in AP which normally accompanied the administration of 50 mU exogenous AVP (group 1). Thus, d(CH2)5VDAVP is a specific antagonist of the vascular effects of AVP. d(CH2)5VDAVP failed to significantly alter AP in water diuretic rats (group 3) and was without effect on urine osmolality during water diuresis or antidiuresis. However, bolus injection of d(CH2)5VDAVP into water deprived rats (group 2) prompted an abrupt fall in AP from 112 +/- 4 to 94 +/- 4 mm Hg (P less than 0.001). This fall in AP was transient, with return of AP to 110 +/- 4 mm Hg within 15 minutes. Administration of saralasin, an angiotensin II antagonist, not only prevented the compensation in AP, but also significantly magnified the maximal hypotensive response seen following d(CH2)5VDAVP (group 4). Discontinuing the saralasin allowed AP to return to baseline. Bilateral nephrectomy (group 5) also prevented the return of AP, further implicating endogenous angiotensin II as the specific mediator of the compensation in AP following d(CH2)5VDAVP administration. These studies clearly demonstrate that circulating AVP contributes to the maintenance of AP during water deprivation in the anesthetized rat. When this vascular action of AVP is blocked, angiotensin II assumes major responsibility for blood pressure regulation in the antidiuretic state.
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PMID:Relative contributions of arginine vasopressin and angiotensin II to maintenance of systemic arterial pressure in the anesthetized water-deprived rat. 700 48

Arginine vasopressin (AVP) stimulates renal prostaglandin (PG) production which is thought to inhibit vasopressins' antidiuretic action. Using rat renal medullary cells in culture (RMIC), we compared the ability of the following peptides which possess different biological activities to stimulate prostaglandin biosynthesis: AVP (high antidiuretic and pressor activities); 1-desamino-8-D-arginine vasopressin (a synthetic peptide with high antidiuretic and no pressor activity); and oxytocin (intermediate pressor, low antidiuretic activity). Radiometric thin-layer chromatography of supernatant media from cells incubated with octatritiated or [14C]arachidonic acid revealed only one radiolabeled peak which co-migrated with PGE2. Radioimmunoassay confirmed that PGE2 was the only prostaglandin synthesized by RMIC. Incubation of cells with AVP (1 nM to 3 microM) increased PGE2 synthesis measured by radioimmunoassay in a concentration-dependent fashion up to 2 1/2-fold over control; 1-desamino-8-D-arginine did not increase PGE2 synthesis. Oxytocin stimulated PGE2 synthesis, but was less potent than AVP. Preincubation of RMIC with [1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid)-4-valine, 8-D-arginine]vasopressin, a synthetic nonpressor, nonantidiuretic antagonists of AVP's pressor activity, completely blocked the ability of AVP to stimulate PGE2 synthesis. We conclude that the ability of AVP to stimulate PGE2 synthesis in RMIC is related to its pressor, not its antidiuretic, activity.
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PMID:The effect of arginine vasopressin and its analogs on the synthesis of prostaglandin E2 by rat renal medullary interstitial cells in culture. 745 79

1. The effects of Na+ on vasopressin release and on redistribution of Ca2+, Na+ and H+ in isolated rat neurohypophysial nerve endings have been studied. 2. Substituting Na+ for a non-permanent cation produced a pronounced and sustained release of vasopressin. This increase occurred in the absence of external Ca2+ and in nerve endings loaded with the Ca2+ chelator dimethyl-BAPTA (1,2-bis-(O-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid). 3. The effect of Na+ was independent of a rise in intracellular Ca2+ as judged by the measurement of [Ca2+]i using the indicator fura-2 and 45Ca2+ efflux studies. Although Na+ could release Ca2+ from internal reservoirs the small elevation in [Ca2+]i induced by Na+ could not explain the large and sustained increase in vasopressin secretion. 4. The channel blockers TTX (tetrodotoxin), D888 (desmethyoxyverapamil), N144 (5-nitro-2-(phenylpropylamino)-benzoic acid) or SITS (4-acetamido-4'-isothiocyanatostilbene-2,2'-disulphonic acid) could not prevent the Na(+)-dependent increase in vasopressin release. Similarly this increase was not affected by metabolic inhibitors (Ruthenium Red and KCN) nor by CCCP (carbonyl cyanide m-chlorophenylhydrazone), an uncoupler of oxidative phosphorylation. 5. Selectivity among monovalent cations to promote secretion was found with the largest effect on the secretory response being produced by Na+. Similarly Cl- was found to be the most potent anion studied for inducing, in the presence of Na+, an increase in neurohormone release. 6. Measuring [Na+]i by means of the Na+ indicator SBFI showed that the extent of the secretory response was correlated with the intraterminal Na+ concentration. 7. The Na(+)-induced, Ca(2+)-independent release of vasopressin occurred by exocytosis as judged (i) by the linear relationship between the amount of vasopressin secreted and that of the co-localized neurophysin and (ii) by the demonstration that the extracellular marker horseradish peroxidase was only found in endocytotic vacuoles and not in the cytoplasm of the stimulated nerve endings. 8. The Na(+)-dependent secretory response found on addition of extracellular Na+ was not the result of the change in internal pH as measured with the indicator BCECF and as mimicked by addition of propionic acid. 9. Addition of Na+ to digitonin- or streptolysin-O-permeabilized nerve endings in the presence or absence of Ca2+ also gave rise to an increase in vasopressin secretion. 10. It is concluded that an increase in internal Na+ per se can promote, in the absence of a rise in intracellular Ca2+, an increase in neuropeptide secretion.
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PMID:Sodium-evoked, calcium-independent vasopressin release from rat isolated neurohypophysial nerve endings. 750 28


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