Abstract: | To examine the effect of aldosterone on sarcolemmalNa+ transport, we measuredouabain-sensitive electrogenicNa+-K+pump current(Ip) involtage-clamped ventricular myocytes and intracellularNa+ activity(aiNa) in right ventricularpapillary muscles. Aldosterone (10 nM) induced an increase in bothIp and the rateof rise of aiNa duringNa+-K+pump blockade with the fast-acting cardiac steroid dihydroouabain. Thealdosterone-induced increase inIp and rate ofrise of aiNa was eliminated bybumetanide, suggesting that aldosterone activates Na+ influx through theNa+-K+-2Cl cotransporter. To obtain independent support for this, theNa+,K+, andCl concentrations in thesuperfusate and solution of pipettes used to voltage clamp myocyteswere set at levels designed to abolish the inward electrochemicaldriving force for theNa+-K+-2Cl cotransporter. This eliminated the aldosterone-induced increase inIp. We concludethat in vitro exposure of cardiac myocytes to aldosterone activates theNa+-K+-2Cl cotransporter to enhance Na+influx and stimulate theNa+-K+pump. |