Hyperaldosteronemia in rabbits inhibits the cardiac sarcolemmal Na+-K+ pump

Aldosterone upregulates the Na+-K+ pump in kidney and colon, classical targ et organs for the hormone. An effect on pump function in the heart is not f irmly established, Because the myocardium contains mineralocorticoid recept ors, we examined whether aldosterone has an effect on Na+-K+ pump function in cardiac myocytes. Myocytes were isolated from rabbits given aldosterone via osmotic minipumps and from controls. Electrogenic Na+-K+ pump current, arising from the 3:2 Na+:K+ exchange ratio, was measured in single myocytes using the whole-cell patch clamp technique. Treatment with aldosterone ind uced a decrease in pump current measured when myocytes were dialyzed with p atch pipette solution containing Na+ in a concentration of 10 mmol/L, where as there was no effect measured when the solution contained 80 mmol/L Nat. Aldosterone had no effect on myocardial Na+-K+ pump concentration evaluated by vanadate-facilitated [H-3]ouabain binding or by K+-dependent paranitrop henylphosphatase activity in crude homoge nates, Aldosterone induced an inc rease in intracellular Na+ activity. The aldosterone-induced decrease in pu mp current and increased intracellular Na+ were prevented by cotreatment wi th the mineralocorticoid receptor antagonist spironolactone. Our results in dicate that hyperaldosteronemia decreases the apparent Na+ affinity of the Na+-K+ pump, whereas it has no effect on maximal pump capacity.