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 effect of papaverine, an inhibitor of the phosphodiesterase responsible for breakdown of cAMP, on the transepithelial sodium transport across the isolated frog skin was investigated. Serosal addition of papaverine caused initially an increase in the short-circuit current (SCC), a doubling of the cellular cAMP content and a depolarization of the intracellular potential under SCC conditions (Vscc). The initial increase in the SCC was followed by a pronounced decrease both in the SCC and in the natriferic action of antidiuretic hormone (ADH), but papaverine had no inhibitory effect on the ability of ADH to increase the cellular cAMP content. As SCC declines, no hyperpolarization was observed. The I/V relationship across the apical membrane during the inhibitory phase, revealed that papaverine reduces the sodium permeability of the apical membrane (PNaa) as well as intracellular sodium concentration. These observations and the previously noted effect of papaverine on Vscc indicates that papaverine must have an effect on the cellular Cl or K permeability. The basolateral Na,K,2Cl cotransporter was blocked with bumetanide, which should bring the cellular chloride in equilibrium. Bumetanide had no effect on basal SCC and Vscc. When papaverine was added to skins preincubated with bumetanide, the effect of papaverine on SCC and Vscc was unchanged. Therefore, the depolarization of Vscc, observed during the papaverine-induced inhibition of the SCC, must be due to a reduction in the cellular K permeability. In conclusion, it is suggested that papaverine reduces the sodium permeability of the apical membrane and the potassium permeability of the basolateral membrane of the frog skin epithelium.
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PMID:Papaverine reduces the sodium permeability of the apical membrane and the potassium permeability of the basolateral membrane in isolated frog skin. 132 Dec 50

The mechanism of transepithelial NaCl transport was investigated in isolated perfused cortical collecting ducts from the kidneys of deoxycorticosterone-treated rats. In the presence of vasopressin, hydrochlorothiazide (0.1 mM) markedly reduced the net rate of Na absorption, Cl absorption, and active fluid absorption but did not significantly change the transepithelial voltage. Similarly, in the absence of vasopressin, hydrochlorothiazide decreased the rate of sodium absorption by 50% without affecting transepithelial voltage. Amiloride (30 microM) completely eliminated the lumen-negative voltage but decreased net sodium absorption only by approximately 50%. In the presence of amiloride, chloride absorption occurred against an electrochemical gradient for chloride, indicating that there was active chloride absorption. Bumetanide (0.1 mM) did not affect chloride absorption or spontaneous fluid absorption in the presence of vasopressin. The combination of amiloride and hydrochlorothiazide inhibited net sodium absorption by a greater extent than did either agent alone. These results demonstrate the presence of the following two parallel sodium transport pathways in cortical collecting ducts from mineralocorticoid-replete rats: 1) an electrogenic pathway blocked by amiloride, which presumably involves an apical sodium channel, and 2) a thiazide-inhibitable electroneutral pathway, which presumably utilizes apical Na-Cl cotransport and mediates secondary active transport of chloride.
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PMID:Thiazide-sensitive NaCl absorption in rat cortical collecting duct. 239 77

The effects of bumetanide on Na transport in the isolated toad urinary bladder were investigated. When applied to the serosal side, this loop diuretic inhibited Na transport. By contrast, when applied to the mucosal side, it stimulated Na transport by increasing the apical Na permeability. These dual effects of bumetanide were also observed with the loop diuretic furosemide. The mucosal action of bumetanide was attributable to release of Na self-inhibition, as evidenced by its dependency on mucosal Na concentration and its interaction with another apical Na permeability stimulator, p-chloromercuriphenyl sulfonate. The stimulatory action of bumetanide was not reduced by the natriferic effect of antidiuretic hormone, but it was totally blockable by the epithelial Na channel blocker amiloride. Bumetanide, however, caused a leftward shift of the concentration-response curve of amiloride on Na current as predicted from its effect on Na self-inhibition. This stimulatory activity of bumetanide and furosemide as demonstrated in the in vitro isolated amphibian epithelia suggests that these loop diuretics also have the potential to stimulate Na transport at the distal portion of the mammalian nephron. Thus, this property of these diuretics might be one of the factors contributing to the observation of increased Na reabsorption along the distal tubule after in vivo administration of furosemide and piretanide as reported in some micropuncture studies.
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PMID:Bumetanide stimulation of sodium permeability of the apical membrane of toad urinary bladder. 284 38

The renal papillary surface epithelium is exposed to pelvic urine on its apical surface and to inner medullary interstitium on its basolateral surface. To investigate transport in this epithelium, we dissected it free from the renal papilla of rabbits and mounted it in a chamber that allowed both sides to be bathed independently. Cell volume was measured at 25 degrees C utilizing computerized quantitative microscopy. Addition of ouabain (10(-4) M) to the basolateral solution induced a 20% volume increase. This volume increase was completely inhibited by the removal of apical bath NaCl, Na+, K+, or Cl- but not by the removal of urea. Bumetanide, down to 10(-9) M in the apical bath, completely inhibited the ouabain-induced swelling. Changes in apical bath osmolality, resulting from addition or removal of NaCl, caused cell volume changes that were greater than could be accounted for by osmotic water flow alone. This hyperresponse was blocked by bumetanide and was stimulated by vasopressin (10(-8) M). These observations are consistent with the presence of Na-K-ATPase in the basolateral membrane and a bumetanide-sensitive, vasopressin-responsive Na-K-Cl co-transporter in the apical membrane.
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PMID:Na-K-Cl cotransport in apical membrane of rabbit renal papillary surface epithelium. 375 57

Extracellular fluid volume is highly regulated, at least in part, by peripheral resistance and renal function. Nitric oxide (NO) produced by NO synthase type 3 (NOS 3) in the nonrenal vasculature may promote fluid retention by reducing systemic vascular resistance and arterial pressure. In contrast, NO produced by renal NOS 3 promotes water excretion by reducing renal vascular resistance, increasing glomerular filtration, and inhibiting reabsorption along the nephron. Thus, the net effect of NO from NOS 3 on urinary volume (UV) is unclear. We hypothesized that NO produced by NOS 3 promotes water excretion primarily due to renal tubular effects. We gave conscious wild-type and NOS 3 -/- mice an acute volume load and measured UV, blood pressure, plasma renin concentration (PRC), Na(+), vasopressin, and urinary Na(+) and creatinine concentrations. To give the acute volume load, we trained mice to drink a large volume of water while in metabolic cages. On the day of the experiment, water was replaced with 1% sucrose, and mice had access to it for 1 h. Volume intake was similar in both groups. Over 3 h, wild-type mice excreted 62 +/- 10% of the volume load, but NOS 3 -/- excreted only 42 +/- 5% (P < 0.05). Blood pressure in NOS 3 -/- was 118 +/- 3 compared with 110 +/- 2 mmHg in wild-type mice (P < 0.05), but it did not change following volume load in either strain. PRC, vasopressin, and glomerular filtration rate were similar between groups. Urinary Na(+) excretion was 49.3 +/- 7.0 in wild-type vs. 37.8 +/- 6.4 mumol/3 h in NOS 3 -/- mice (P < 0.05). Bumetanide administration eliminated the difference in volume excretion between wild-type and NOS 3 -/- mice. We conclude that 1) NO produced by NOS 3 promotes water and Na(+) excretion and 2) the renal epithelial actions of NO produced by NOS 3 supersede the systemic and renal vascular actions.
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PMID:Nitric oxide produced by endothelial nitric oxide synthase promotes diuresis. 2014 12