RESUMEN
In the heart, two types of calcium currents were described, the L-and T-type. In addition to these two types, a dihydropyridine-resistant Ca[2+] component has been described to be up-regulated in rat ventricular cardiomyocytes during their differentiation-dedifferentiation process. The aim of our study is to examine if such calcium current component is present in human cardiomyocytes. The patch clamp technique was used to record Ca[2+] current in atrial cells. In the presence of 2 micro M nifedipine, residual current was activated [-2.7 +/- 0.7 pA/pF, n=6] in the same voltage range as the L-type, nifedipine-sensitive Ca[2+] current [-2.1 +/- 0.4 pA/pF, n=6], but its steady-state inactivation was negatively shifted by 10 mV. This nifedipine-resistant Ca[2+] current was completely blocked by 500 micro M cadmium chloride and significantly enhanced by 1 micro M isoproterenol [-7.5 +/- 0.5 pA/pF, n=6; p <0.01]. These results give evidence that a nifedipine-resistant Ca[2+] current, similar to the one which has been shown to be developmentally expressed in rat ventricular cardiomyocytes, is observed in human atrial cells. Its molecular identity, its expression level as well as its role in pathophysiologic conditions remain to be studied