Am J Physiol Cell Physiol Journal of Applied Physiology
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Am J Physiol Cell Physiol 274: C175-C181, 1998;
0363-6143/98 $5.00
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Vol. 274, Issue 1, C175-C181, January 1998

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

Anastasia S. Mihailidou1, Kerrie A. Buhagiar1,2, and Helge H. Rasmussen1,2

Department of Cardiology, 1 Royal North Shore Hospital, and 2 University of Sydney, Sydney, New South Wales 2065, Australia

To examine the effect of aldosterone on sarcolemmal Na+ transport, we measured ouabain-sensitive electrogenic Na+-K+ pump current (Ip) in voltage-clamped ventricular myocytes and intracellular Na+ activity (aiNa) in right ventricular papillary muscles. Aldosterone (10 nM) induced an increase in both Ip and the rate of rise of aiNa during Na+-K+ pump blockade with the fast-acting cardiac steroid dihydroouabain. The aldosterone-induced increase in Ip and rate of rise of aiNa 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 Ip. 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.

ion transport; intracellular sodium; sodium-potassium-two chloride cotransport; mineralocorticoid receptor; cell membrane


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