Na+ influx and Na+-K+pump activation during short-term exposure of cardiac myocytes to aldosterone.

To examine the effect of aldosterone on sarcolemmal Na+ transport, we measured ouabain-sensitive electrogenic Na+-K+pump current ( I p) in voltage-clamped ventricular myocytes and intracellular Na+ activity ([Formula: see text]) in right ventricular papillary muscles. Aldosterone (10 nM) induced an increase in both I p and the rate of rise of [Formula: see text] during Na+-K+pump blockade with the fast-acting cardiac steroid dihydroouabain. The aldosterone-induced increase in I p and rate of rise of [Formula: see text] was eliminated by bumetanide, suggesting that aldosterone activates Na+ influx through the Na+-K+-2Cl-cotransporter. To obtain independent support for this, the Na+, K+, and Cl- concentrations in the superfusate and solution of pipettes used to voltage clamp myocytes were set at levels designed to abolish the inward electrochemical driving force for the Na+-K+-2Cl-cotransporter. This eliminated the aldosterone-induced increase in I p. We conclude that in vitro exposure of cardiac myocytes to aldosterone activates the Na+-K+-2Cl-cotransporter to enhance Na+influx and stimulate the Na+-K+pump.