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 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

The mucosal surface of toad urinary bladder was examined with scanning electron microscopy following its exposure to 20 mU/ml of vasopressin (VP), 10(-4) M 8-bromo-cAMP, 1 mM acetylcholine chloride, serosal hypertonicity, or a hypotonic bathing medium. After a 30-min exposure to VP, the arborizing ridge-like surface pattern typical of granular cells was transformed into microvilli, a response that was not dependent on transepithelial osmotic water movement. An identical response occurred following a 30-min exposure of the bladder to 8-bromo-cAMP, again in the absence of an osmotic gradient. Microvillus formation was not observed when cell volume was increased by incubation of tissue in half-normal amphibian Ringer's solution for 30 min, or with exposure to acetylcholine, which caused accentuation of the convexity of the apical surface of the granular cell similar to that observed with VP-induced osmotic water flow. However, 60 min of incubation in a hypertonic serosal medium (mannitol, 240 mM) caused transformation of ridges to microvilli mimicking the picture obtained with VP. These findings establish that transepithelial osmotic water flow with cell swelling is not required for microvillus formation on the apical surface of granular cells following VP stimulation, and that the surface changes are not due to cell swelling alone or to changes in the configuration of the apical plasmalemma. The results also suggest that the response to VP is mediated via the generation of cAMP. Finally, this study demonstrates that serosal hypertonicity also causes transformation of ridges to microvilli by a mechanism that is yet to be defined.
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PMID:Effect of vasopressin and serosal hypertonicity on toad urinary bladder. 23 89

In cardiopulmonary bypass the effect on plasma vasopressin levels of the addition of whole blood to the pump priming solution was measured. Six patients (Group I) had blood added to the lactated Ringer's solution for the prime, and six patients (Group II) had only lactated Ringer's solution. Neither group had significant changes in plasma vasopressin levels until surgical stimulation occurred. Comparable significant elevations occurred during bypass in both groups. Greater decreases in haematocrit and urinary K+ and greater increases in urinary Na+ occurred in Group II. The degree of haemodilution does not appear to effect plasma vasopressin levels but may alter the degree of electrolyte shift.
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PMID:Plasma vasopressin levels during cardiopulmonary bypass with and without profound haemodilution. 66 69

We demonstrate that salts of diatrizoate and iothalamate, radiographic contrast agents, depress the active transport of sodium in the urinary bladder of the Columbian toad, Bufo marinus. Isolated toad bladders were incubated in isotonic Ringer's solutions with isosmolar displacement of sodium chloride by contrast media in experimental solutions. Sodium transport as measured both by short-circuit current (SCC) and by isotopic sodium flux was significantly depressed in the presence of sodium diatrizoate. Sodium transport measured by SCC was significantly depressed with sodium iothalamate and meglumine iothalamate. Equimolar methylsulfate Ringer's solution did not depress SCC. Although contrast media in isotonic Ringer's solutions depressed basal SCC, the vasopressin-stimulated increment in SCC was not depressed by contrast media. Separate experiments with hyperosmolar solutions (786 mM, as utilized in angiography) demonstrated equivalent suppression of SCC by contrast media and by other solutions made hyperosmolar with glucose or sodium methylsulfate, implying a general or nonspecific effect of hyperosomolarity. Inhibition of SCC by contrast media was reversible when the agents were removed by serial changes with standard Ringer's solution. Inhibition of sodium transport by contrast media might provide a basis for studies on some of the clinical toxicities of these agents.
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PMID:Inhibition of active sodium transport by radiographic contrast media. 80

Cadmium ion (Cd++) significantly increased potential difference (PD) and short-circuit current (SCC) across isolated frog skin when added to the outside Ringer's solution at 10(-4), 10(-3) and 5 X 10(-3) M concentration. Resistance was reduced by 10(-4) 7 cd++ but not significantly changed by the higher concentrations. When SCC was first stimulated by vasopressin, 10(-4) and 10(-3) M Cd++ produced additive stimulation which was reversible by washing with Cd++-free Ringer's. If SCC was first stimulated by Cd++, further stimulation by vasopressin was additive with 10(-4)M Cd++ but dompletely inhibited by 10(-3)M Cd++. Elevating the calcium ion (Ca++) concentration of the outer Ringer's from 10(-3) M to 5 X 10(-3)M or 10(-2)M prior to Cd++ treatment did not reduce the magnitude of SCC stimulation by Cd++. Removal of Ca++ from the outside Ringer's with 2 X 10%-3)M EDTA increased SCC as predicted. Subsequent addition of 5 X 10(-3) M Cd++ drastically reduced SCC below control levels while equimolar concentrations of Cd++ and EDTA reduced SCC only to control levels. These results suggest that Cd++ interacts with the components of the apical plasma membranes of epithelial cells which are associated with the stimulation of SCC by vasopressin and Ca++ removal and may be a useful probe for elucidating these components.
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PMID:Effects of Cd++ on short-circuit current across epithelial membranes. I. Interactions with Ca++ and vasopressin on frog skin. 81 28

Pressor amine therapy in circulatory shock has been generally unfavorable, presumably because these drugs produce unselective, intense vasoconstriction and curtail rather than improve true capillary inflow, distribution and outflow in the microcirculation. The present study compares the influence of a new analog of vasopressin, [2-phenylalanine, 8-ornithine]vasopressin (POV), over wide dose ranges and Ringer's solution on: 1) survival after circulatory shock, induced by different means (e.g., hemorrhage, bowel ischemia); 2) blood pressure and hematocrit in shocked animals; and 3) various microcirculatory parameters after induction of hemorrhage and bowel ischemia shock (e.g., lumen diameters of various types of microvessels, reactivity of microvessels, microvascular flow patterns, leukocytic sticking, petechial hemorrhage formations, vasomotion, etc.). Local administration of POV, in contrast to constrictor catecholamines, induces a venular-to-arteriolar profile of constrictor activity in the normal rat mesenteric microcirculation. Systemic administration of POV to rats subjected to either lethal hemorrhage or bowel ischemia shock: 1) increases survival rates 2- to 8-fold over control rats receiving Ringer's solution; 2) produces a plateau-like effect on arterial blood pressure and returns arterial hematocrits toward normal after hemorrhage; and 3) regenerates and sustains vasomotion and venular tone, decreases microvascular hyper-reactivity characteristic of shock syndromes, restores constricted arteriolar lumen sizes toward normal, predisposes to a splanchnic microbed virtually free of stasis and petechiae, and restores capillary perfusion and outflow to near-normal. These findings indicate that it is possible to synthesize vasoactive molecules which exert selective microvascular effects and are highly beneficial in therapy of low-flow states.
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PMID:Microcirculatory approach to the treatment of circulatory shock with a new analog of vasopressin, (2-phenylalanine, 8-ornithine)vasopressin. 93 6

Ethanol (3%) decreases the potential difference and short-circuit current across the isolated frog skin in chloride Ringer's solution. Unidirectional fluxes of Na and Cl indicate that the drop in short-circuit current is due to an inhibition of the sodium influx. However, ethanol had no effect on the electrical parameters or sodium fluxes, when the frog skin was bathed in chloride-free solutions on both sides or the outside alone. The ethanol response is anion-dependent. In addition, chloride-free media in the inside bathing solution reduced the short-circuit current, indicating a sodium transport pathway which is dependent on chloride and confirming previous data in the literature. Other anions such as sulfate and nitrate could not substitute for chloride. The vasopressin-induced natriferic response and the ethanol effect were found to work independently of each other and different pathways of action are suggested for these agents. The intracellular sodium content of the isolated frog skin epithelium increased and potassium decreased in the presence of the Na-K adenosine triphosphatase inhibitor, ouabain, whereas ethanol or amiloride had no effect. The oxygen consumption of the isolated frog skin was unaffected by up to 10% ethanol. A general metabolic action is probably thus not mediating the response. Urea, in iso-osmotic concentrations to the ethanol, did not mimic its effect. Tritiated water fluxes (in the absence of an osmotic gradient) were reduced by 30% in the presence of 3% ethanol. It is suggested that ethanol may impede the flow of water across frog skin by a physicochemical interaction with membrane pores and the water molecules. The permeability coefficient (Ktrans) for ethanol was found to be 10 times smaller than the Ktrans for water.
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PMID:Effects of ethanol on the permeability of frog skin. 108 5

Acute volume expansion was produced in 9 dogs by infusing a lactated Ringer's solution at 1 ml/kg/min in a volume estimated to increase blood volume by 20%. Volume expansion was maintained by replacing urinary fluid losses with equal volumes of the Ringer's solution. Following volume expansion, the effects of a slow, nonhypotensive hemorrhage on plasma antidiuretic hormone concentration (PADH) were determined and compared to a group of 9 normovolemic dogs subjected to the same hemorrhage procedure, in order to determine if volume receptor control of ADH release would adapt to acute increases in blood volume. Ringer's infusion significantly increased blood volume to 95.2 +/- 3.1 ml/kg (mean +/- SE; P less than 0.01) when compared to a mean normovolemic blood volume of 77.6 +/- 3.4 ml/kg. Volume expansion was associated with a significantly lower PADH (3.2 +/- 1.6 muU/ml) than that in normovolemic dogs (5.7 +/- 1.2 muU/ml; p less than 0.05). Significant increases in PADH (P less than 0.05) occurred in both groups of dogs after 20 and 40 minutes of a continuous, nonhypotensive hemorrhage (0.40 to 0.45 mg/kg/min. Hemmorrhage was also associated with significant decrease in effective left atrial pressure in both groups of dogs after 5, 10, 20, and 40 minutes of hemorrhage (P less than 0.01). There were no significant differences between the two groups of dogs nor were there any significant changes during the experiment within each group for mean arterial blood pressure, arterial pulse pressure, plasma osmolality, plasma sodium concentration and plasma potassium concentration. Effective left atrial pressure and PADH were found to be exponentially correlated with blood volume in bothy hypervolemic and normovolemic dogs. Analysis of covariance of these correlations suggested that the hypervolemic dogs exhibited the same exponential changes in PADH and effective left atrial pressure with decreased blood volume as in the normovolemic dogs. It is concluded that acute volume expansion does not alter volume control of plasma ADH concentration.
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PMID:Volume control of plasma antidiuretic hormone concentration following acute blood volume expansion in the anesthetized dog. 119 3

Norepinephrine alters the transepithelial electrical properties of an open-circuited urinary bladder from the mud puppy, Necturus maculosus. When 10(-5) M norepinephrine is superfused over the serosa of the epithelium, the transepithelial voltage (Vt) and short-circuit current (Isc) increase as the resistance (Rt) decreases. The norepinephrine-mediated changes are reversed by the addition of amiloride (5.10(-5) M) to the mucosal Ringer's solution. The serosal adrenoceptors mediating the Na+ transport are more sensitive to norepinephrine (EC50 = 1.2.10(-6) M) than to epinephrine or isoproterenol. Since the Isc is blocked selectively by the antagonist, phenoxybenzamine, stimulation of active transepithelial Na(+)-flux by catecholamines is mediated by an alpha-adrenoceptor. The apical cell membrane voltage (Va) and fractional resistance (fRa) were recorded using conventional KCl-filled microelectrodes. Untreated tissues have Va close to 0 mV while the basolateral membrane voltage (Vb) is between -85 and -95 mV. About 90% of Rt is apical cell membrane resistance (fRa). When amiloride inhibits sodium transport, Va becomes negative, Vb hyperpolarizes slightly and fRa increases to 97%. On the other hand, if the bladders are treated with norepinephrine, fRa decreases to 79% as Va becomes positive and Vb depolarizes. When Rt changes, the resistance of the paracellular pathway (Rp) is unaltered. Changes in the electrical properties of the tissue appear to be mediated primarily by alterations in Ra. Since the Necturus bladder does not respond to antidiuretic hormone, this study implies that biogenic amines regulate Na+ transport in the epithelium.
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PMID:Norepinephrine stimulation of sodium transport in Necturus urinary bladder. 230 5

In a search for factors contributing to the sustained blood pressure (BP) elevation in acutely volume-loaded animals, dextran dissolved in lactated Ringer's solution (20 ml/kg) was infused into 34 mongrel dogs over a period of 1 hour under pentobarbital anesthesia and changes in hemodynamic and humoral variables were monitored during its infusion and for 3 hours after its infusion. BP elevation during volume loading (from 114 +/- 3 to 128 +/- 3 [SEM] mm Hg) was attributed to an increase in cardiac output. After volume loading, some dogs maintained BP elevation whereas others did not. The former group showed an increase in total peripheral resistance, demonstrating a transformation of cardiac output to total peripheral resistance as a responsible factor in maintenance of the elevated BP. The plasma levels of norepinephrine, vasopressin, and plasma renin activity were not elevated, indicating that these vasoactive factors were not responsible for elevation of the BP or total peripheral resistance. The changes in the hematocrit, atrial natriuretic factor, urine volume, and urinary sodium excretion were identical in the two groups, and natriuresis was not prominent when total peripheral resistance was high. Pressor responses to norepinephrine and angiotensin II were potentiated 3 hours after stopping infusion in both groups, but this potentiation was not correlated with the increase in total peripheral resistance or mean BP. Thus, acute volume expansion produced resistance-dependent hypertension following the initial volume-dependent hypertension. It is unlikely that a vascular sensitizing natriuretic factor plays a role in the resistance-dependent BP elevation. The mechanism and physiological importance of hypersensitivity to vasoactive substances remain to be elucidated.
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PMID:Vasoconstriction and hypersensitivity to vasoactive substances after acute volume expansion in dogs. 245 68


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