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1 INSERM U-637; UM1, CHU Arnaud de Villeneuve, 34295 Montpellier, France
2 Département de Pharmacologie et de Toxicologie, Université de Lausanne, CH-1005 Lausanne, Switzerland
3 INSERM AVENIR, IFR 52, Collège de France, 75231 Paris, France
Aldosterone is involved in a variety of pathophysiological processes that ultimately cause cardiovascular diseases. Despite this, the physiological role of aldosterone in heart function remains elusive. We took advantage of transgenic mouse models characterized by a renal salt-losing (SL) or salt-retaining (SR) phenotype, thus exhibiting chronically high or low plasma aldosterone levels, respectively, to investigate the chronic effects of aldosterone in cardiomyocytes devoid of pathology. On a diet containing normal levels of salt, these animals do not develop any evidence of cardiovascular disease. Using the whole cell patch-clamp technique on freshly isolated adult ventricular cardiomyocytes, we observed that the amplitude of L-type Ca2+ currents (ICa) correlates with plasma aldosterone levels. Larger values of ICa are associated with high aldosterone concentrations in SL models, whereas smaller values of ICa were observed in the SR model. Neither the time- nor the voltage-dependent properties of ICa varied measurably. In parallel, we determined whether modulation of ICa by blood concentration of aldosterone has a major physiological impact on the excitation–contraction coupling of the cardiomyocytes. Action potential duration, [Ca2+]i transient amplitude and contraction are increased in the SL model and decreased in the SR model. In conclusion, we demonstrate that the blood concentration of aldosterone exerts chronic regulation of ICa in mouse cardiomyocytes. This regulation has important consequences for excitation–contraction coupling and, potentially, for other Ca2+-regulated functions in cardiomyocytes.
(Received 15 June 2005;
accepted after revision 8 September 2005;
first published online 15 September 2005)
Corresponding author J.-P. Benitah: INSERM U-637, UM1, CHU Arnaud de Villeneuve, 34295 Montpellier, France. Email: benitah{at}montp.inserm.fr
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