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)

The adenylate-cyclase activator forskolin, the guanylate-cyclase stimulator sodium nitroprusside, the phosphodiesterase inhibitor Ro 15-2041, different Ca-entry blockers, as well as various vasodilators, and the atrial natriuretic peptide were tested for antiplatelet activity. Thrombin, vasopressin, ADP, arachidonic acid, and the dihydropyridine Ca agonist CGP 28392 were used as platelet activators. The physiological and biochemical parameters of platelet function studied included shape-change reaction, intracellular free-Ca modulation, and cyclic nucleotide formation. When inhibition of the shape-change response occurred, it was accompanied by inhibition of the increase in intracellular free Ca. Furthermore, the results suggest a possible intracellular site of action of Ca entry blockers in platelets, and confirm the importance of modulation of cyclic nucleotides in the regulation of platelet function, regardless of the mechanism of platelet activation. Additional antiplatelet activity of antihypertensive agents may have a beneficial effect in reducing the associated risk of thrombo-embolic complications in essential hypertension.
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PMID:Vasodilating agents and platelet function: intracellular free calcium concentration, cyclic nucleotides, and shape-change response. 243 9

Acidification of the medium bathing the serosal surface of the toad urinary bladder results in impairment of the water permeability response to vasopressin. The magnitude of the hydrosmotic response to a maximal concentration of either vasopressin or the cyclic nucleotide analogue 8-(p-chlorophenylthio)-cyclic 3',5'-adenosine monophosphate (C1PhS-cAMP) was progressively reduced when serosal bath pH was decreased from 8.5 to 6.5. The disulfonic stilbenes SITS and DIDS and the diuretic furosemide, agents known to interfere with anion transport and with the regulation of intracellular pH in other tissues, inhibited the water flow response to vasopressin and C1PhS-cAMP in a pH-dependent manner when added to the serosal bathing medium. Inhibition of the hydrosmotic response to 10(-5) M C1PhS-cAMP was estimated to be half-maximal at 1.5 X 10(-4) M SITS, 2 X 10(-5) M DIDS, and 1 X 10(-5) M furosemide. The degree of inhibition induced by the anion transport inhibitors varied inversely with the concentration of exogenous cyclic nucleotide. SITS, DIDS, and furosemide had no effect on either basal or vasopressin-stimulated short-circuit current at serosal pH 8.5; all three agents inhibited basal short-circuit current at pH 7.1 but had no effect on the natriferic response to vasopressin. These results are consistent with the view that changes in intracellular hydrogen ion and/or anion concentration can selectively inhibit the increase in water permeability elicited by vasopressin at a step(s) distal to the generation of cAMP.
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PMID:Anion transport inhibitors: effects on water and sodium transport in the toad urinary bladder. 298 47

We investigated by micropuncture the effects of glucagon and parathyroid hormone (PTH) on thin limbs of juxtamedullary nephrons of rats with reduced plasma concentration of endogenous glucagon, PTH, antidiuretic hormone (ADH) and calcitonin, all four hormones enhancing the adenylate-cyclase activity in the thick ascending limbs and the distal nephron. Such a hormonal depletion suppresses the corticomedullary concentration gradient, making favourable conditions for studying the influence of these hormones on the renal concentrating mechanism. Administration of glucagon (4.4 ng/min-1) or PTH (5 mU/min-1) to these hormone-deprived rats elicited the expected decrease in urinary Mg and Ca fractional excretion without modifying either fractional or absolute excretion of water. At the tip of the loop, glucagon enhanced the loop fluid osmolality by 20%, but left the delivery of water unchanged. The Na and Cl concentrations increased significantly with the osmolality, resulting in a positive correlation between the fractional delivery of either ion and the loop fluid osmolality. PTH increased the fraction of filtered phosphate delivered to the thin limbs, as expected, but, in contrast to glucagon, did not alter either the Na, Cl, or total solute fractional deliveries. The Mg, Ca and K deliveries were unaffected by glucagon and PTH. In conclusion, glucagon, which activates the cyclase system of both the medullary and cortical portion of the thick ascending limb, enhances the delivery of salt to the tip of the loop by net sodium chloride addition to the descending limb. PTH which activates the adenyl-cyclase system only in the cortical thick ascending limb cannot enhance such NaCl delivery. NaCl, when added, might therefore originate from the medullary thick ascending limb.
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PMID:Effects of glucagon and PTH on the loop of Henle of rat juxtamedullary nephrons. 371 66

The effects of synthetic human calcitonin (HCT) on water and electrolyte deliveries to the thin limbs of Henle's loop of juxtamedullary nephrons were investigated by micropuncture in the rat. To avoid undesirable interference with exogenous calcitonin, experiments were performed in hormone-deprived rats with reduced circulating calcitonin, antidiuretic hormone, parathyroid hormone and glucagon, all four of which stimulate the adenylate-cyclase activity in the thick ascending limb and the distal tubule. Administration of HCT (1.0 mU/min X 100 g body wt) to such rats significantly reduced the urinary fractional excretion rate of water, Mg, Ca and K. At the tip of the longlooped nephrons, the fractional delivery of water diminished in the presence of HCT, although the glomerular filtration rate of these nephrons was unaltered. Simultaneously, the loop fluid osmolality rose significantly. HCT, however, did not alter the fraction of total filtered solutes remaining in the thin limbs, nor the NaCl fractional delivery. As previously observed in this laboratory with dDAVP, the reduced fractional delivery of water at the hairpin turn was accompanied by a decrease in Mg and Ca deliveries in rats given HCT, indicating that the handling of these two ions along the descending limb may be linked in part to the water movements in this nephron segment. The fractional deliveries of K at the hairpin turn and in urine were significantly correlated, and both decreased in the presence of HCT. Since, as shown previously, HCT reduces the net addition of K along the superficial distal tubule, it is concluded that calcitonin inhibits the medullary recycling of K between the nephron terminal segments and the loop of Henle of juxtamedullary nephrons.
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PMID:Effects of human calcitonin on water and electrolyte movements in rat juxtamedullary nephrons: inhibition of medullary K recycling. 371 48

1 Single lobes of the bladder of Bufo marinus were isolated and filled with, and suspended in, oxygenated Ringer solution. The fluid in contact with the outside (serosa) of the lobes had a total osmolarity of 225 m-osmol/litre, and that bathing the inside (mucosa) of 45 m-osmol/litre.2 Osmotic water flow from mucosa to serosa was measured by weighing the lobes every 30 minutes. It was negligible unless vasopressin was added to the serosal bath. Standard concentrations of either 1.25 or 6.25 mu/ml were used to render the bladder lobes permeable to water.3 The presence in the serosal medium of pentobarbitone or thiopentone in concentrations ranging from 0.25 to 2.5 mM, or of chloralose in concentrations ranging from 0.65 to 6.5 mM, diminished the increase in water permeability induced by vasopressin.4 The three anaesthetics exerted similar inhibitory effects on the action of vasopressin from the serosal and from the mucosal surface of the bladder.5 In the presence of a constant high concentration of anaesthetic, increasing the concentration of vasopressin over three orders of magnitude led to stepwise increases of osmotic water flow out of the lobes, although at every dose level the effect of vasopressin was depressed by the anaesthetic. However, it was not completely abolished even if the concentration of vasopressin was close to threshold.6 The increase in water permeability of the bladder induced by 3',5'-adenosine monophosphate (cyclic AMP) was also depressed by the three anaesthetics.7 Possible explanations of the findings are discussed.
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PMID:The influence of anaesthetics on the increase in the water permeability of the toad bladder induced by vasopressin. 420 91

1. The effects of antidiuretic hormone (ADH), theophylline and cyclic 3',5'-adenosine monophosphate (AMP) on membrane potentials in frog skin have been investigated.2. Membrane potentials across the outer and inner facing membranes were recorded in both normal and current clamped skins. In the latter condition active transport of sodium had been abolished by ouabain or metabolic inhibitors, but ionic gradients were maintained by passing current through the skin from the inside.3. ADH increases the potential across the outer facing membranes and reduces the skin resistance. The results are consistent with ADH causing an increase in permeability of the outer facing membranes to sodium ions.4. Theophylline reduces the skin potential by reducing specifically the potential across the outer facing membranes. At the same time the skin resistance is reduced. Theophylline acts by increasing the permeability of the outer facing membranes to chloride ions.5. Cyclic 3',5'-AMP causes a biphasic potential change accompanied by an increase in skin resistance.6. Metabolic inhibitors block the response of the skin to ADH but not to theophylline.7. Separate explanations for the increase in sodium transport by ADH, theophylline and cyclic 3',5'-AMP are discussed. It is not necessary to involve cyclic AMP in order to explain the effects of either ADH or theophylline.
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PMID:Independent action of antidiuretic hormone, theophylline and cyclic 3',5'-adenosine monophosphate on cell membrane permeability in frog skin. 430 35

1. Amiloride reduces short-circuit current and potential difference across the isolated frog skin.2. Isotopically measured sodium influx and efflux are diminished.3. Total electrical conductance and partial sodium conductance are diminished, the reduction in total conductance being entirely accounted for by the reduction in partial sodium conductance.4. The effect of antidiuretic hormone (ADH), cyclic 3'5'-adenosine monophosphate (cyclic AMP) and theophylline can be antagonized by pretreatment with amiloride but the antagonism can be abolished by increasing the concentration of these compounds.5. Amiloride has no effect on oxygen consumption in concentrations which inhibit sodium transport. However, it prevents the stimulatory effect of ADH on oxygen consumption.6. The results are consistent with an action of amiloride at the passive outside membrane of the transporting cells of isolated frog skin.
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PMID:Effects of amiloride on active sodium transport by the isolated frog skin: evidence concerning site of action. 431 93

The effects of several prostaglandins (PG) and a highly purified preparation of cholera enterotoxin (CT) on intestinal mucosal adenyl cyclase activity and the effect of CT on intestinal mucosal cyclic 3',5'-adenosine monophosphate concentration were determined in guinea pig and rabbit small intestine and were correlated with the effects of the same agents on ion transport. Adenyl cyclase activity, measured in a crude membrane fraction of the mucosa, was found at all levels of the small intestine with the highest activity per milligram protein in the duodenum. The prostaglandins, when added directly to the assay, increased adenyl cyclase activity; the greatest effect (2-fold increase) was obtained with PGE(1) (maximal effect at 0.03 mM) and PGE(2). The prostaglandins also increased short-circuit current (SCC) in isolated guinea pig ileal mucosa, with PGE(1) and PGE(2) again giving the greatest effects. The prior addition of theophylline (10 mM) reduced the subsequent SCC response to PGE(1) and vice versa. It was concluded, therefore, that the SCC response to PGE(1), like the response to theophylline, represented active Cl secretion. CT increased adenyl cyclase activity in guinea pig and rabbit ileal mucosa when preincubated with the mucosa from 1 to 2.5 hr in vitro or for 2.5 hr in vivo but not when added directly to the assay. The increments in activity caused by PGE(1) and NaF were the same in CT-treated and control mucosa. Cyclic 3',5'-AMP concentration in rabbit ileal mucosa was increased 3.5-fold after a 2 hr preincubation with CT in vitro. Phosphodiesterase activity in the crude membrane fraction of the mucosa was unaffected by either CT or PGE(1). A variety of other agents including insulin, glucagon, parathormone, thyroid-stimulating hormone, L-thyroxine, thyrocalcitonin, vasopressin, and epinephrine all failed to change adenyl cyclase activity. It is concluded that CT and certain prostaglandins produce small intestinal fluid secretion by increasing mucosal adenyl cyclase activity, thereby stimulating an active secretory process.
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PMID:Stimulation of intestinal mucosal adenyl cyclase by cholera enterotoxin and prostaglandins. 432 9

The isolated urinary bladder of the toad responds to neurohypophyseal hormone with a net increase of water transport from the mucosal to the serosal solution in the presence of an osmotic gradient. This response is mediated intracellularly by cyclic 3',5'-adenosine monophosphate (AMP). The present study demonstrates that hydroosmotically active substances such as oxytocin, dibutyryl cyclic 3',5'-AMP, and theophylline, but not hydroosmotically inactive substances, induce the uptake of horseradish peroxidase from the mucosal solution. Peroxidase taken up by the mucosal cells is demonstrable in small tubules and vesicles, and eventually accumulates in lysosomes. The uptake of peroxidase from the serosal solution into similar bodies in the mucosal cells is not hormone-dependent. It is also shown that peroxidase does not penetrate the tight junction from either the mucosal or serosal solution. These results extend previous findings which implicated the apical membrane of the mucosal epithelium as the site affected by neurohypophyseal hormones. A mechanism based on secretory phenomena is proposed as a framework for future investigations of apical membrane permeability changes and pinocytosis.
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PMID:Correlation between pinocytosis and hydroosmosis induced by neurohypophyseal hormones and mediated by adenosine 3',5'-cyclic monophosphate. 432 55

Vasopressin increased adenyl cyclase activity in homogenates of both inner and outer renal medulla of the rat. It also increased the concentration of cyclic 3',5'-adenosine monophosphate (AMP) in slices of both inner and outer medulla but not in renal cortex. In the inner medulla, a concentration of prostaglandin E(1) (PGE(1)), which was ineffective by itself significantly reduced the stimulation of adenyl cyclase activity and cyclic AMP concentration induced by vasopressin. These results are consistent with the hypothesis that PGE(1) can compete with vasopressin for adenyl cyclase-binding sites. However, the findings in the outer medulla suggest the situation is more complex. Although 10(-8) M PGE(1) had no effect by itself and inhibited the vasopressin-induced elevation of cyclic AMP, larger amounts of PGE(1) increased both adenyl cyclase activity and cyclic AMP levels. The maximum effect on the latter parameter was at least 6 times as great as that of maximum amounts of vasopressin.
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PMID:Effects of vasopressin and prostaglandin E 1 on the adenyl cyclase-cyclic 3',5'-adenosine monophosphate system of the renal medulla of the rat. 433 95


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