Characterization of voltage-gated calcium currents in freshly isolated smooth muscle cells from rat tail main artery

The aim of the present study was to characterize voltage-gated Ca2+ current s in smooth muscle cells freshly isolated from rat tail main artery in the presence of 5 mmol L-1 external Ca2+. Calcium currents were identified on t he basis of their voltage dependencies and sensitivity to nifedipine, Ni2and cinnarizine. In the majority of the cells studied, T- and L-type curren ts were observed, while the remaining cells showed predominantly L-type cur rents. In the latter group of cells, holding potential change from -50 to e ither -70 or -90 mV increased the corresponding inward current amplitude wh ile its voltage activation threshold remained uncharged. The steady state i nactivation of L-type Ca2+ channels showed half-maximal inactivation at -38 mV. A Ca2+ dependent inactivation was also evident. Nifedipine (3 mu mol L -1) blocked L-type but not T-type Ca2+ currents. Ni2+ (50 mu mol L-1) as we ll as cinnarizine (1 mu mol L-1) suppressed the nifedipine-resistant, T-typ e component of the currents. At higher concentrations, both Ni2+ (0.3-1 mmo l L-1) and cinnarizine (10 mu mol L-1) blocked the net inward current. Repl acement of Ca2+ with 10 mmol L-1 Ba2+ significantly increased the amplitude of L-type Ca2+ currents. These results demonstrate that smooth muscle cell s freshly isolated from rat tail main artery may be divided into two popula tions, one expressing both L- and T-type and the other only L-type Ca2+ cha nnels. Furthermore, this report shows that in arterial smooth muscle cells cinnarizine potently inhibited T-type currents at low concentrations (1 mu mol L-1) but also blocked L-type Ca2+ currents at higher concentrations (10 mu mol L-1).