Role of K(+) channels in the regulation of electrical spontaneous activity of the mouse small intestine

Abstract

The roles of K(+) channels in the regulation of slow waves and pacemaker potentials recorded from mouse small intestine were investigated using intracellular recording techniques in the presence of nifedipine. Iberiotoxin (0.1 microM) and charybdotoxin (0.1 microM) had no effect on the generation of slow waves recorded from circular smooth muscle cells. Apamin (0.3 microM) depolarized the membrane and decreased the amplitude of early, rapid repolarization of slow waves, without altering the amplitude, frequency, duration, or maximum rate of rise of the initial upstroke phase (dV/dt(max)). The early, rapid repolarization was enhanced by phenylephrine (15 microM). 4-Aminopyridine (4-AP, 5 mM) depolarized the membrane and increased the amplitude and dV/dt(max) of slow waves. Both apamin and 4-AP depolarized the membrane and decreased the amplitude and dV/dt(max) of pacemaker potentials recorded from interstitial cells of Cajal distributed in the myenteric region (ICC-MY). Membrane depolarization with a high-K(+) solution decreased the amplitude and dV/dt(max) of slow waves. These results suggest that apamin-sensitive K(+) conductance and 4-AP-sensitive K(+) conductance may contribute to the resting membrane potential of circular smooth muscle cells. The early, rapid repolarization of slow waves appears to result from the opening of apamin-sensitive K(+) conductance. 4-AP-sensitive K(+) conductance is likely to be activated in the initial upstroke component (primary component) of slow waves. In ICC-MY, membrane depolarization induced by apamin or 4-AP may result from electrotonic spread from smooth muscle cells.