Na+ influx and Na(+)-K+ pump activation during short-term exposure of cardiac myocytes to aldosterone.
Am J Physiol
; 274(1): C175-81, 1998 01.
Article
en En
| MEDLINE
| ID: mdl-9458726
ABSTRACT
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 (alpha iNa) in right ventricular papillary muscles. Aldosterone (10 nM) induced an increase in both Ip and the rate of rise of alpha iNa during Na(+)-K+ pump blockade with the fast-acting cardiac steroid dihydroouabain. The aldosterone-induced increase in Ip and rate of rise of alpha iNa 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.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Músculos Papilares
/
Sarcolema
/
Sodio
/
ATPasa Intercambiadora de Sodio-Potasio
/
Aldosterona
Límite:
Animals
Idioma:
En
Año:
1998
Tipo del documento:
Article