RESUMO
Natriuretic peptides seem to be a potent regulator of cell Ca[2+] signaling in their action on the cardiovascular system. It was therefore the aim of this study to investigate the effect[s] of B-type natriuretic peptide [BNP] on the action potential and the L-type calcium current [I[cal]] in the rat left ventricular myocytes. Perforated and whole cell patch clamp technique was used to record action potential [AP] and I[cal] in current and voltage clamp mode, respectively. At the concentration tested of 10[-7] M, BNP significantly increased the action potential duration at 50% and at 90% of repolarization by 16.85% and 16.39% respectively, and the phase II slope of the AP by 52.5% ; reduced the I[cal] amplitude with a 16.17% decrease in the peak amplitude ; reduced [16.51%] the inactivation time course of current decay; increased the V[0.5] activation of the L-type calcium channel by 32.84% and decreased V[0.5] inactivation by 34.39%. These data suggest that BNP modulates cardiomyocyte function by reducing I[cal] and modifying the AP. This study may show a novel facet to evaluate the paracrine/autocrine effect of BNP on the normal heart function
RESUMO
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