Two roles of calcium during the spike in circular muscle of small intestine in cat

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Abstract
Small bundles (100-250 .mu.m) of circular muscle were subjected in the double sucrose gap to current and voltage clamp. Regenerative action potentials with amplitudes greater than 60 mV above the resting level were observed in 44% of the bundles. Reduction of the external concentrations of Ca decreased spike amplitude, while Na replacement with Li or tetramethylammonium [TEA] had little effect. Ca conductance blockers Mn (1-2 mM), and verapamil and D600 [methoxyverapamil] (10-5 M) eliminated spiking. Spike amplitude was increased and the rate of repolarization was decreased by tetraethylammonium or substitution of Ba for Ca. Under voltage clamp, both Ca and Ba were effective in carrying an inward current transient. With large depolarizing steps, a transient outward current was seen whose time course overlapped that of the inward current. Lowering [Ca]o reduced both the inward and outward current transients; elimination of both transients followed exposure to Mn. The outward transient alone was eliminated by TEA or Ba-Krebs. Activation of the outward transient seems to require an influx of Ca; Ba is incapable of activating the outward transient. The reversal potential for the outward current was shifted to a more positive level in high K and this was taken as evidence, along with the effects of TEA, that the ion responsible for the outward transient current was K. Following the elimination of the Ca-activated K conductance change by Ba substitution, a small voltage-dependent late outward current was observed. Steady-state current-voltage curves showed, in the depolarizing quadrant, an inward-going rectification and with further depolarization an outward-going rectification.