NA-K+ PUMP ACTIVATION DURING SHORT-TERM EXPOSURE OF CARDIAC MYOCYTES TO ALDOSTERONE( INFLUX AND NA+)

To examine the effect of aldosterone on sarcolemmal Na+ transport, we measured ouabain-sensitive electrogenic Na+-K+ pump current (I-p) in v oltage-clamped ventricular myocytes and intracellular Na+ activity (a( Na)(i)) in right ventricular papillary muscles. Aldosterone (10 nM) in duced an increase in both I-p and the rate of rise of a(Na)(i) during Na+-K+ pump blockade with the fast-acting cardiac steroid dihydroouaba in. The aldosterone-induced increase in I-p and rate of rise of a(Na)( i) was eliminated by bumetanide, suggesting that aldosterone activates Na+ influx through the Na+-K+-2Cl(-) cotransporter. To obtain indepen dent support for this, the Na+, K+, and Cl- concentrations in the supe rfusate and solution of pipettes used to voltage clamp myocytes were s et at levels designed to abolish the inward electrochemical driving fo rce for the Na+-K+-2Cl(-) cotransporter. This eliminated the aldostero ne-induced increase in I-p. We conclude that in vitro exposure of card iac myocytes to aldosterone activates the Na+-K+-2Cl(-) cotransporter to enhance Na+ influx and stimulate the Na+-K+ pump.