Using the whole-cell mode path-clamp techniques at 20~23℃, membrane currents were recorded from single smooth muscle cells enzymatically isolated from the rabbit gastric antrum. Outward currents were activated with a threshold around-30mV and
carried
by K+, which showed apparent outward rectification.
The outward current was potentiated by high(4 mM) calcium, but reduced by EGTA and cadmium in bath solution. The outward current was potentiated by caffeine above-10 mV by test pulses, however, not changed below -10mV. External TEA(2~4mV)
inhibited
the
outward current ina concentration-dependent manner. The outward current was slightly increased by 4-AP(5mM) above -10 mV by test pulse but decreased below -10 mV in normal Tyrode solution. In the presence of 10 mM TEA to block outward K+ current,
the
residual outward current was further blocked by 4-AP on the whole voltage range of test pulses. Outward K+ current could be divided into two components : (1) a Ca2+-activated K+ current component and (2)a delayed rectifier K+ current component.
Ca2+-activated K+ current was Ca2+- and voltage-dependent oscillatory current. It was blocked by TEA of low concentration and slightly increased by 4-AP. Delayed rectifier K+ current was Ca2+-independent, but voltage-dependent and it was
insensitive to
TEA(2~4 mM) and could be blocked by 4-AP in the presence of TEA(10 mM) to block Ca2+-activated K+ current. When Mg2+ was applied extracellularly or into intrapipette solution, outward K+ currents were decreased in a dose-dependent manner and the
degree
of block was increased with depolarization. Ca2+-activated K+ current was potentiated by elevation of extracellular calcium but this potentiation had bell-shaped concentration dependency. External barium, which was known to block the K+ currents,
potentiated Ca2+- activated K+ current in normal Tyrode solution. But it blocked the residual outward current in the presence of 10mM TEA to block Ca2+-activated K+ current.
The above results suggested that magnesium might have blocked outward K+ current by inhibiting the Ca2+-activated K+ current and the calcium-induced calcium release. And calcium increased the Ca2+- activated K+ current up to 2~4 mM and then
decreased it
probably by the calcium channel inactivation in higher concentration. Barium might have been a charge carrier for Ca2+-activated K+ current and blocked only the delayed rectifier K+ current.
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