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 Ca(2)(+) currents (I(Ca)) correlates with plasma aldosterone levels. Larger values of I(Ca) are associated with high aldosterone concentrations in SL models, whereas smaller values of I(Ca) were observed in the SR model. Neither the time- nor the voltage-dependent properties of I(Ca) varied measurably. In parallel, we determined whether modulation of I(Ca) by blood concentration of aldosterone has a major physiological impact on the excitation-contraction coupling of the cardiomyocytes. Action potential duration, [Ca(2)(+)](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 I(Ca) in mouse cardiomyocytes. This regulation has important consequences for excitation-contraction coupling and, potentially, for other Ca(2)(+)-regulated functions in cardiomyocytes.