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 NA-K-ATPase of toad skin was characteristically sensitive to Na, K, and ATP. It was not affected by amiloride, vasopressin, cAMP, and thyroxine, but stimulated by insulin. Ouabain, a potent inhibitor at 37 degrees C, did not inhibit the enzyme activity significantly at 23 degrees C. The optimal pH for the enzyme activity increased as temperature decreased. However, the optimal OH-/H+ ratio of the medium remained constant at 16 regardless of temperature. The Km for ATP remained unchanged between 37 and 8 degrees C if the OH-/H+ ratio was held constant at 16, but increased as temperature decreased if the pH of the medium was held constant at 7.4. The enzyme activity showed no appreciable variation between 37 and 20 degrees C with a constant OH-/H+ ratio of 16, whereas it decreased logarithmically at a constant pH of 7.4 over the same temperature range. These results indicate the presence of a typical Na-K-ATPase system in toad skin and that the enzyme is in the most active catalytic state at a fixed level of OH-/H+ ratio in the medium regardless of incubation temperature.
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PMID:Properties of toad skin Na-K-ATPase with special reference to effect of temperature. 1 98

Toad bladder epithelial cells were isolated under mild conditions in a calcium-free medium; they were found to exclude trypan blue, to consume oxygen, and to respond to vasopressin with an increased rate of oxygen consumption. Since isolated toad bladder epithelial cells are mostly spherical in shape, the cell diameter can be accurately measured with an ocular micrometer of an inverted microscope. Epithelial cells swelled by 29+/-3% in the presence of KCN. This cyanide-induced swelling of cells was prevented by amiloride or, alternatively, by replacing NaCl by equiosmotic amounts of mannitol in the Ringer's fluid. Cells incubated in the presence of vasopressin swelled by 10+/-2%. Vasopressin and KCN acted synergistically in enhancing cell volume. Ouabain caused cells to swell by 9+/-2%, and this effect was not additive to the swelling seen with vasopressin. These observations are in accord with the theory of Leaf and his associates, that the predominant effect of vasopressin is to enhance sodium entry into the transporting epithelial cells of the toad urinary bladder.
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PMID:Action of vasopressin, ouabain, and cyanide on the volume of isolated toad bladder epithelial cells. 40 62

1. Simultaneous measurements of unidirectional sodium fluxes across foetal skin incubated in vitro with identical solutions ([Na] = 150 mM) bathing either side showed a flux ratio (influx/efflux) of 1-40+/-0-08 in twenty-seven sheep skins, which was significantly different from unity (P less than 0-001). The gestational ages ranged from 47 to 98 days (term = 147 days). Similar experiments on eight foetal pig skins at 58 days gestation (term = 114-118 days) gave a mean flux ratio of 1-10 +/- 0-03 (P less than 0-02). 2. Unidirectional sodium fluxes measured with dilute Ringer solution on the outside (mucosal) surface ([Na]0 = 100mM) gave influx to efflux ratios of 0-86 +/- 0-09 in seventeen sheep (P less than 0-05) and 1-07 +/- 0-26 in five foetal pigs; the value predicted for passive movement was 0-67. 3. Incubation with inhibitors, ouabain (10-4 M) or dinitrophenol (DNP) (10-4 M) gave a flux ratio for sodium which was not significantly different from unity in the absence of a gradient, or from 0-67 when the concentration gradient was applied. 4. Sequential measurement of unidirectional diffusional fluxes of tritiated water across foetal skin gave flux ratios of 0-98 +/- 0-02 in six sheep skins and 1-06 +/- 0-11 for four pig skins in control conditions. When the outside solution was diluted to give an osmotic gradient of 100 m-osmole. kg-1 across the skin a flux ratio of 0-95 +/- 0-07 was obtained for seven sheep and was not measured in pig skin. Hormones and inhibitors had no effect on the diffusional flux ratio for water in the presence or absence of an osmotic gradient. 5. Lysine vasopressin (ADH) (200 mu./ml.) increased influx and efflux of water in the presence and, to a lesser extent in the absence of an osmotic gradient in sheep skin. In pig skin prolactin (1 u./ml.) increased both influx and efflux, but ADH had no effect on diffusional water fluxes. 6. ADH increased sodium influx in sheep skin slightly but vasotocin (5-5 mu./ml.) was more potent, particularly in the presence of an opposing diffusion gradient. Vasotocin (55 mu./ml.) reduced sodium influx in pig skin ADH had no effect on influx or efflux and prolactin reduced sodium influx and efflux. Ouabain and DNP generally reduced permeability to both sodium and water in sheep skin but had no effect in pig skin.
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PMID:Active sodium uptake by the skin of foetal sheep and pigs. 95 62

The effects of ouabain, vasopressin, and furosemide on intracellular concentrations of total sodium([Na]) and potassium [K]), on exchangeable sodium ([Na]) and the sodium transport pool ([Nap]) were investigated in isolated short circuited skins of rana esculenta. Furosemide was added to the epithelial bathing solution, vasopressin and ouabain to the corial bathing solution. Results were compared with the amount of net sodium transport measured by short circuit current (scc). Ouabain reduces scc and increases [Na] and [Na]; [K] is decreased. The administration of vasopressin leads to a sharp increase of scc, combined with an enhancement of of [Na] and [Na]; [K] shows no significant change. [Nap] is significantly increased, too, and approximately to the same amount as [Na]. Furosemide causes an increase of scc, whereas a significant change of [Na], [Na] and [K] could not be detected. On the other hand, [Nap] was enhanced significantly. The results support the hypothesis that furosemide like vasopressin is acting by increasing the entry of sodium into the transport compartment of the active cell layer. The result is an increased transfer of sodium across the skin.
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PMID:Effects of furosemide on sodium content and transport pool in frog skin (Rana esculenta): comparison with vasopressin and ouabain. 108 Dec 3

We compared the effects of the phosphodiesterase inhibitor amrinone, the beta-adrenergic partial agonist xamoterol and the digitalis glycoside, ouabain, on isolated rabbit hearts perfused with the Langendorff technique. Heart rate, left ventricular pressure, as an index of myocardial contractility and coronary perfusion pressure, as an index of coronary resistances, were assessed before and after each drug. Perfusion with concentrations of each agent varying from 10(-9) to 10(-4) M induced a dose-dependent increase of left ventricular systolic pressure averaging 32.5 +/- 1.5% after amrinone (10(-5) M), 46.2 +/- 0.5% after xamoterol (10(-5) M) and 19.0 +/- 2.1% after ouabain (10(-4) M). Among the 3 agents, only amrinone was able to reduce basal coronary perfusion pressure (18.4 +/- 1.2% at the dose of 10(-5) M) and inhibit vasopressin-induced coronary spasm (86.8 +/- 2.5% inhibition at 10(-5) M); no significant change of coronary perfusion pressure was noted with either xamoterol or ouabain. Heart rate was not significantly modified by amrinone whereas, at the doses of 10(-5)-10(-4) M, xamoterol increased it by 21.6 +/- 0.7% and ouabain reduced it by 12.3 +/- 1.1%. Our results show that amrinone, in comparison with digitalis glycosides and beta-adrenergic agonists, presents the unique property to increase myocardial contractility with concomitant coronary vasodilation without significant changes of heart rate. Ouabain has a less potent positive inotropic activity and a slight negative chronotropic action, whereas xamoterol inotropic effect is accompanied by an increase of heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of amrinone on isolated heart preparations: comparative study with other inotropic agents]. 168 91

The mechanism of ion transport across principal cells of rat cortical collecting tubules (CCT) and its regulation by vasopressin (ADH) has been studied in the isolated perfused tubule. To amplify the response to ADH rats were treated with 5 mg I. M. desoxycorticosterone 4-9 days prior to the experiments. Addition of 2 X 10(-10) mol X l-1 ADH increased the transepithelial voltage from -5.1 +/- 0.7 mV to -16.1 +/- 1.4 mV (n = 37) and decreased the transepithelial resistance from 51 +/- 4 omega cm2 to 39 +/- 2 omega cm2 (n = 33). Optical and functional differentiation of impalements of principal and intercalated cells was made and only data of principal cells are presented. ADH depolarized the apical membrane from 79 +/- 1 mV to 66 +/- 2 mV (n = 26) and decreased the fractional resistance of the apical membrane from 0.76 +/- 0.04 to 0.70 +/- 0.04 (n = 13). These ADH effects were prevented by 10(-5) or 10(-4) mol X l-1 luminal amiloride which hyperpolarized the apical membrane when added in the presence or absence of ADH. Apical and basolateral membranes were dominated by large K+ conductances and addition of 3 mmol X l-1 barium to bath or lumen perfusates increased transepithelial resistance almost two-fold, whereas luminal amiloride increased the transepithelial resistance only by 26-35%. Ouabain (0.5 mmol X l-1, bath) depolarized the basolateral membrane and decreased its K+ conductance. These effects were prevented by the simultaneous presence of apical amiloride suggesting that the only route of Na+ entry into the principal cells occurred via the amiloride sensitive Na+ conductance. We conclude that ADH stimulates Na+ reabsorption and K+ secretion in the rat CCT primarily by increasing the Na+ conductance in the apical cell membrane.
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PMID:Electrophysiological studies in principal cells of rat cortical collecting tubules. ADH increases the apical membrane Na+-conductance. 244 57

1. Isolated neurosecretory nerve endings were prepared from rat neurohypophyses. The amount of vasopressin (AVP) and oxytocin released was measured by radioimmunoassay. 2. The amount of hormone release under resting conditions was not affected by external calcium (Ca2+o). Secretion decreased by ca. 50% when external sodium (Na+o) was replaced by choline or sucrose. 3. Ouabain did not modify the basal AVP release. 4. The Na+ ionophore monensin increased the release of AVP only in the presence of Na+o. This increase was maintained during prolonged exposure to the ionophore and occurred in the presence of Ca2+o only. 5. In the presence of Ca2+o, the amount of evoked hormone release was dependent on the external K+ concentration. Half-maximal activation was achieved with ca. 40 mM-K+. The K+-induced secretion was potentiated in Na+-free solution. 6. Prolonged 100 mM-K+-induced depolarization in the presence of Ca2+o gave rise to a large increase in hormone secretion which decreased with time (t1/2 = 2.5 min). The release could be reactivated after permeabilization of the nerve terminals in the presence of micromolar concentrations of Ca2+. 7. A stepwise paradigm in which Ko+ is incrementally increased to 25, 50, 75 and then 100 mM released more AVP than a prolonged exposure to 100 mM-K+. 8. Veratridine increased the amount of AVP released. This effect was considerably reduced in the absence of Nao+ and abolished in the presence of D600. 9. The depolarization-induced AVP release was blocked by different Ca2+-antagonists. Their effectiveness was nitrendipine = nicardipine greater than Cd2+ greater than Gd3+ greater than Co2+ = Mn2+. 10. The dihydropyridine Bay K 8644 potentiated both the basal and the K+-evoked AVP release. Its maximal effect was obtained with 25-50 mM-Ko+. 11. In conclusion, the isolated neurohypophysial terminals which have both Na+ and Ca2+ channels and release AVP and oxytocin upon depolarization might be an excellent system to study further the mechanisms leading to secretion of neurohormones.
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PMID:Hormone release from isolated nerve endings of the rat neurohypophysis. 245 Sep 99

Ouabain-sensitive 86Rb+ uptake by isolated rat hepatocytes was studied to elucidate how Ca2+-mobilizing hormones stimulate the Na+-pump. Stimulation of this uptake was observed with concentrations of vasopressin ([8-arginine]vasopressin, AVP), angiotensin II, and norepinephrine which elicited Ca2+ mobilization and phosphorylase activation. These results suggested that changes in cytosolic Ca2+, mediated by inositol trisphosphate, might trigger sodium pump stimulation by AVP. However, in hepatocytes incubated in Ca2+-free Krebs-Henseleit buffer, Na+-pump activity was not altered over 15 min by either 1.5 mM EGTA or 1.5 mM Ca2+. Furthermore, incubation of cells in 5 mM EGTA for 15-30 min drastically impaired the ability of AVP to increase cytosolic Ca2+, but only modestly attenuated AVP-stimulated Na+-pump activity. Two tumor promoters, phorbol myristate acetate (PMA) and mezerein, stimulated Na+/K+-ATPase-mediated transport activity. Similarly, addition of synthetic diacylglycerols or of exogenous phospholipase C from Clostridium perfringens to increase endogenous diacylglycerol levels also resulted in a stimulation of the Na+-pump in the absence of changes in cytosolic or total cellular Ca2+ levels. Stimulation of the Na+-pump by the combination of maximal concentrations of PMA and AVP did not produce an additive response, and both agents displayed a transient time course, suggesting that the two agents share a common mechanism. Stimulation of the Na+-pump by AVP and PMA was not blocked by amiloride analogs which inhibit Na+/H+ exchange, but these compounds blocked the action of insulin. These data suggest that the elevated Na+/K+-ATPase-mediated transport activity observed in hepatocytes following exposure to Ca2+-mobilizing hormones is a consequence of stimulated diacylglycerol formation and may involve protein kinase C.
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PMID:The hormone-sensitive hepatic Na+-pump. Evidence for regulation by diacylglycerol and tumor promoters. 302 43

We have characterized a Na+-K+-Cl- cotransporter in vascular endothelial cells (EC) cultured from different blood vessels and species that is inhibited by the diuretics furosemide and bumetanide (50% inhibitory concentration for 86Rb influx approximately 20 microM and 0.5 microM, respectively). Inward 86Rb influx mediated via this pathway is greater than 86Rb influx transported by the Na+-K+ pump in cultured EC from bovine and pig aorta, bovine vena cava, and baboon cephalic vein but not in human umbilical or saphenous vein EC. External Na+ or Cl- -stimulated, ouabain-insensitive 86Rb influx is equal to furosemide or bumetanide-sensitive 86Rb influx. Ouabain-insensitive 22Na influx is also partially inhibited by these drugs and stimulated by increasing external K+ or Cl-. Net Na+ extrusion occurs via the Na+-K+-Cl- cotransporter in the absence of external K+, whereas net Na+ influx occurs at higher external K+ (greater than 1 mM). Maximal concentrations (100 nM) of bradykinin and vasopressin increase the initial rate of bumetanide-sensitive 86Rb influx by approximately 60 and 70% (50% effective concentration approximately 1 and 0.6 nM, respectively). Addition of either ethyleneglycol-bis(beta-aminotethylether)-N,N'-tetraacetic acid or LaCl3 (to block calcium influx) prevents bradykinin-stimulated 86Rb influx. When intracellular calcium is elevated using ionomycin (100 nM), a Ca2+ ionophore, bumetanide-sensitive 86Rb influx increases approximately twofold. In contrast, isoproterenol (100 microM) and forskolin (50 microM), adenylate cyclase stimulators, decrease furosemide-sensitive 86Rb influx.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bradykinin and vasopressin stimulate Na+-K+-Cl- cotransport in cultured endothelial cells. 371 30

The cells of perfused rabbit collecting tubules swell and the intercellular spaces widen during osmotic flow of water from lumen to bath induced by antidiuretic hormone (ADH). Ouabain had no influence on these changes. In the absence of net water flow intercellular width was unaffected when tubules were swollen in hypotonic external media. Therefore, during ADH-induced flow widening of intercellular spaces is not a consequence of osmotic swelling of a closed intercellular compartment containing trapped solutes, but rather is due to flow of solution through the channel. Direct evidence of intercellular flow was obtained. Nonperfused tubules swollen in hypotonic media were reimmersed in isotonic solution with resultant entry of water into intercellular spaces. The widened spaces gradually collapsed completely. Spaces enlarged in this manner could be emptied more rapidly by increasing the transtubular hydrostatic pressure difference. In electron micrographs a path of exit of sufficient width to accommodate the observed rate of fluid flow was seen at the base of the intercellular channel. It is concluded that the intercellular spaces communicate with the external extracellular fluid and that water, having entered the cells across the luminal plasma membrane in response in ADH, leaves the cells by osmosis across both the lateral and basilar surface membranes.
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PMID:Paths of transtubular water flow in isolated renal collecting tubules. 578 74


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