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

Anastasia S. Mihailidou, Kerrie A. Buhagiar, Helge H. Rasmussen*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

56 Citations (Scopus)


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 (a(Na)/(i)) in right ventricular papillary muscles. Aldosterone (10 nM) induced 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 dihydro-ouabain. 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 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.

Original languageEnglish
JournalAmerican Journal of Physiology - Cell Physiology
Issue number1 43-1
Publication statusPublished - Jan 1998
Externally publishedYes


  • Cell membrane
  • Intracellular sodium
  • Ion transport
  • Mineralocorticoid receptor
  • Sodium-potassium-two chloride cotransport


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