Abstract
Two types of voltage-dependent inward currents were evoked by depolarization in murine antral smooth muscle cells (SMCs) bathed in Ca(2+)-containing physiological solution: high-voltage-activated (HVA) and low-voltage-activated (LVA) inward currents. We examined whether the LVA current was due to: 1) T-type Ca(2+) channels, 2) Ca(2+)-activated Cl(-)channels, 3) nonselective cation channels (NSCC), or 4) voltage-dependent K(+) channels. Replacement of external Ca(2+) (2 mM) with equimolar Ba(2+) increased the amplitude of the HVA current but blocked the LVA current. Nicardipine blocked the HVA current, and in the presence of nicardipine, T-type Ca(2+) blockers failed to block LVA current. A Cl(-) channel antagonist had little effect on LVA current. Cation-free external solution completely abolished both HVA and LVA currents. Addition of Ca(2+) to the solution restored only HVA currents. Addition of K(+) (5 mM) to otherwise cation-free solution induced LVA current that reversed at -20 mV. These data suggest that LVA current is not due to T-type Ca(2+) channels, Ca(2+)-activated Cl(-) channels, or NSCC. A-type K(+) (K(A)) currents and delayed rectifying K(+) (K(DR)) currents can be resolved in antral SMCs dialyzed with a solution containing 140 mM K(+). When cells were exposed to high K(+) external solution and dialyzed with Cs(+)-rich solution in the presence of nicardipine, LVA current was evoked and reversed at positive potentials. LVA currents were blocked by K(+) channel blockers, 4-aminopyridine, and tetraethylammonium. In conclusion, LVA inward currents can be generated by K(+) influx via K(A) channels in murine antral SMCs when cells were dialyzed with Cs(+)-rich solution.