Inhibition of rat cardiac and renal Na+,K+-ATPase by high sodium concentrations and vanadate.
In the present study, rat renal Na+,K+-ATPase was found to be more sensitive to inhibition by high Na+ concentrations (100-400 mM) than was rat cardiac Na+,K+-ATPase. K+ was more effective in reversing the inhibition by Na+, of cardiac relative to renal Na+,K+-ATPase. Rat renal Na+,K+-ATPase was also more sensitive than cardiac Na+,K+-ATPase to inhibition by vanadate over this range of Na+ concentrations. These results support the hypothesis that vanadate may selectively regulate Na+,K+-ATPase in the kidney, and they may also help explain the natriuretic and diuretic effects of vanadate in rats. Inhibition of renal Na+,K+ATPase by Na+, may also help explain, in part, the natriuretic and diuretic effects of acute saline loading.
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D000818:Animals; D004347:Drug Interactions; D066298:In Vitro Techniques; D007668:Kidney / Q000201:enzymology*; D008297:Male; D009206:Myocardium / Q000201:enzymology*; D009928:Organ Specificity; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000494:pharmacology*; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors*; D014638:Vanadates; D014639:Vanadium / Q000494:pharmacology*
D014639:Vanadium; D014638:Vanadates; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium