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)

In cell-free preparations (washed 600 x g pellets) of human renal medulla, glucagon produced a dose-dependent stimulation of adenylate cyclase. The stimulation of renal medullary adenylate cyclase by saturating concentrations of glucagon was additive to the saturating doses of vasopressin. Furthermore, L-isoproterenol stimulated renal medullary adenylate cyclase in a dose-dependent manner, and this stimulation was blocked by DL-propranolol. Stimulation of the renal medullary adenylate cyclase by maximal doses of glucagon and L-isoproterenol was additive. DL-Propranolol did not inhibit stimulation of glucagon. Thus, the results indicate the existence of a specific adenylate cyclase that is responsive to glucagon--distinct from the isoproterenol-sensitive adenylate cyclase and the previously described vasopressin-sensitive adenylate cyclase in human renal medulla. We suggest that the renal tubular effect of glucagon may be mediated by glucagon-dependent cyclic-AMP production in renal tissue.
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PMID:Glucagon-sensitive adenylate cyclase in human renal medulla. 0 66

Secretory granules isolated from ox neurohypophyses released their content of vasopressin in the presence of ATP and Mg2+. A half maximal ATP concentration of 0.25 mM was found. Ca2+ was not necessary for the effect. High concentrations of ADP, AMP and ITP were shown to mimic the effect of ATP. Utilizing this effect of ATP combined with iodonitrotetrazolium treatment to make mitochondria heavier, a method is described to obtain granule "ghosts" in a purified form. They were shown to be phosphorylated when granules were incubated with [gamma-32P] ATP.
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PMID:ATP-induced release of vasopressin associated with phosphorylation of isolated bovine neurohypophyseal secretory granule membranes. 2 18

Stimulation of urea and water transport by vasopressin (ADH) appears to occur via independent pathways. We examined the effects of altering serosal or mucosal bath pH on transport of water, urea, and sodium. Compared to bladders with a serosal bath pH of 7.4 to 8.0, reducing the serosal bath pH to 6.8 led to a 60% fall in ADH-stimulated osmotic water flow, without decreasing the permeability of urea. Raising the serosal pH to 9.5 had the opposite effect: urea permeability was inhibited by 40% without altering water flow. Exogenous cyclic AMP-stimulated water and urea permeabilities were not dissociated, but were changed in the same direction by alterations in serosal pH: serosal acidification enhanced the effect of exogenous cyclic AMP on both urea and water, whereas the cyclic AMP effect on both was diminished by serosal alkalinization. This was especially marked for urea, suggesting that an alteration in the urea response to cyclic AMP may be particularly important in defining vasopressin-stimulated urea permeability as the serosal bath pH is altered. Mucosal acidification increased short circuit current but decreased both the urea and water response to ADH and 8-bromo-cyclic AMP. The response to cyclic AMP was less consistent. Mucosal alkalinization did not cause significant changes in either basal or stimulated transport. The data demonstrate distinct and separable effects of bath pH alterations on each of the transport systems examined.
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PMID:pH-Dependence of water and solute transport in toad urinary bladder. 3 88

Intrarenal infusion of somatostatin in anesthetized dogs produced a prompt increase in urine flow in association with a decrease in urinary osmolality and an increase in free water clearance. These changes occurred in the absence of changes in arterial pressure, renal plasma flow, osmolar clearance, electrolyte excretion or cyclic AMP excretion. The diuretic effect occurred primarily in the infused kidney indicating a direct intrarenal action rather than suppression of vasopressin secretion. This diuretic action of somatostatin may result from inhibition of the action of vasopressin on the renal medulla but other possible mechanisms cannot be excluded.
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PMID:An intrarenal effect of somatostatin on water excretion. 4 71

The ability of somatostatin to modify the water premeability of the toad bladder was examined. Somatostatin had a small effect on basal water flow and antagonized the hydrosmotic effect of vasopressin. Water flow induced by cyclic AMP was enhanced. These results may explain the diuretic and hyposthenuric effects of somatostatin in vivo.
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PMID:Antagonism of vasopressin-induced water flow by somatostatin. 10 4

In the urinary bladder of amphibia, hypertonicity of the serosal bath (SH) evokes an increase in transepithelial water permeability, the characteristics of which resemble the response to antidiuretic hormone (ADH). The ionic dependency, in particular for Ca2+, appears very similar for SH- and ADH-induced water fluxes. In the present experiments La3+ was used as a probe to study the Ca2+-dependency of the hydrosmotic response to SH in isolated urinary bladder of the toad Bufo marinus. Addition of La3+ (5 mM) on the serosal side of the membrane produced a significant and reversible increase in basal transepithelial water flux. The hydrosmotic response elicited by adding 250 mM mannitol to the serosal Ringer's solution was inhibited by 30% in the absence of serosal Ca2+. Similarly, the hydrosmotic response to SH was inhibited by 37%, 30% and 40% when 5 mM La3+ was added to the serosal medium 30 min before, concommitantly with, or 60 min after induction of SH. The inhibition of transepithelial water flux observed in the absence of serosal Ca2+ or in the presence of serosal La3+ was reversible. The results support a critical role for Ca2+ in the modulation of transepithelial water permeability in the urinary bladder of amphibia. Ca2+ presumably exerts its effects at a post-cyclic AMP step.
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PMID:Reversible inhibition by lanthanum of the hydrosmotic response to serosal hypertonicity in toad urinary bladder. 11 63

Subcellular distribution of the enzymes related to the cellular action of antidiuretic hormone was studied in bovine renal medulla. The highest activity of vasopressin-stimulated adenylate cyclase was found in plasma membranes. The basal activity increased two times above homogenate while vasopressin-stimulated and NaF-stimulated activities both increased five times. Adenylate cyclase activity was present also in other particulate fractions, but it was not significantly stimulated by vasopressin. Cyclic AMP phosphodiesterase was predominantly located in the cytosol when assayed with 0.5 mM cyclic AMP or with 5 muM cyclic AMP. However, with the latter concentration of cyclic AMP more activity remained associated with the particulate fractions and was more inhibited by theophylline. The highest cyclic AMP-stimulated protein kinase activity occurred in the cytosol. Protein kinase activity present in other subcellular fractions was not markedly stimulated by cyclic AMP. Protein phosphatase activity was highest in cytosol when assayed using 32P-histones, 32P-plasma membrane proteins, and 32P-cytoslic proteins. The activity was unaffected by 10-6M to 10-4M cyclic AMP or cyclic GMP. The activity was completely inhibited by 10mM ZnSO4 and 10mM CuSO4; 10mM NaF inhibited the activity by approximately 14%. The enzymes related to the cellular action of vasopressin are predominatly localized in the cytosol except for the vasopressin-sensitive adenylate cyclase which is plasma membrane bound. To mediate the effect of antidiuretic hormone and act on the luminal plasma membrane these soluble enzymes and their substrates should be compartmentalized, possibly by a system of cytoplasmic microtubules.
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PMID:Subcellular distribution of the enzymes related to the cellular action of vasopressin in renal medulla. 16 75

Cyclic AMP accumulates in the Ringer solution bathing the toad urinary bladder in vitro. At least 4 times more cyclic AMP is released into the solution bathing the serosal surface than into the solution bathing the mucosal surface. Most of the cyclic AMP originates in the epithelial cells rather than the stroma. Vasopressin increased the content of cyclic AMP in the epithelial cells and increases the amount of cyclic AMP in the Ringer solution. Since there is not an increase in medium cyclic AMP when cell cyclic AMP levels are increased by theophylline, it is suggested that theophylline may reduce the permeability of the cell membrane to cyclic AMP. Finally, it is demonstrated that 10 mM NaF increase the amount of cyclic AMP in the epithelial cells and in the solution bathing the bladder, but block the effect of vasopressin on water permeability, presumably at a step subsequent to the formation of cyclic AMP.
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PMID:Release of cyclic AMP by toad urinary bladder. 16 96

Patients treated with lithium salt have an inability to concentrate urine, possible due to the inhibition of the antidiuretic effect of vasopressin. Since beta adrenergic stimulation also induces antidiuresis, a possible effect of lithium on the catecholamine-induced antidiuresis was investigated in dog kidneys. The urinary concentrating ability induced by the iv injection of isoproterenol 0.1 mug/kg was markedly inhibited in the lithium-treated animals (plasma lithium 1.13 plus or minus 0.10 mM). The increase of cyclic AMP concentration by 1 muM isoproterenol was also significantly less in the renal medullary slices obtained from the lithium-treated animals than in those obtained from the control animals. These findings suggest that the inability to concentrate urine in the patients treated with lithium salt is probably due to the inhibition of the antidiuretic effect of catecholamine as well as that of vasopressin; and the inhibitory mechanism of lithium on the catecholamine-induced antidiuresis is possibly through the inhibition of the catecholamine-dependent cycle AMP system in renal medulla.
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PMID:Effect of lithium on catecholamine-induced antidiuresis and cyclic AMP in dog kidneys. 16 36

Na+-K+-ATPase was inhibited by 1 times 10-4M ethacrynic acid and mercuderamide, and by 1 times 10-3M hydrochlorothiazide and furosemide. A modification of Gilman's (1970) protein displacement assay has been used to measure c-AMP levels in toad bladder epithelial cells. Vasopressin (50 mU/ml) caused c-AMP levels to rise from 4.27 to 9.27 pmol/mg protein. Ethacrynic acid had no effect on cellular c-AMP levels after 10 min exposure to the drug, but at 90 min caused a reduction of both basal and vasopressin stimulated levels. Furosemide caused an apparent rise in c-AMP levels, dilution ratio measurements indicated interference by this drug in the assay procedure, mecuderamide also caused substantial interference with the c-AMP assay. Hydrochlorothiazide had no effect on basal or hormone stimulated levels of c-AMP. It was concluded that the inhibition of sodium transport produced by ethacrynic acid in toad bladder is probably due to inhibition of adenylate cyclase, an effect not shared by other dieuretics.
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PMID:The effect of diuretics on Na+-K+-ATPase and c-AMP levels in toad bladder epithelial cells. 16 90


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