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

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Abstract
The aim of the present study was to characterize voltage-gated Ca2+ currents 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 the basis of their voltage dependencies and sensitivity to nifedipine, Ni2+ and cinnarizine. In the majority of the cells studied, T- and L-type currents were observed, while the remaining cells showed predominantly L-type currents. In the latter group of cells, holding potential change from –50 to either –70 or –90 mV increased the corresponding inward current amplitude while its voltage activation threshold remained unchanged. The steady state inactivation of L-type Ca2+ channels showed half-maximal inactivation at –38 mV. A Ca2+-dependent inactivation was also evident. Nifedipine (3 μmol L–1) blocked L-type but not T-type Ca2+ currents. Ni2+ (50 μmol L–1) as well as cinnarizine (1 μmol L–1) suppressed the nifedipine-resistant, T-type component of the currents. At higher concentrations, both Ni2+ (0.3–1 mmol L–1) and cinnarizine (10 μmol L–1) blocked the net inward current. Replacement of Ca2+ with 10 mmol L–1 Ba2+ significantly increased the amplitude of L-type Ca2+ currents. These results demonstrate that smooth muscle cells freshly isolated from rat tail main artery may be divided into two populations, one expressing both L- and T-type and the other only L-type Ca2+ channels. Furthermore, this report shows that in arterial smooth muscle cells cinnarizine potently inhibited T-type currents at low concentrations (1 μmol L–1) but also blocked L-type Ca2+ currents at higher concentrations (10 μmol L–1).