Abstract

The influence of nicotine on potassium (⁴²K) exchange in denervated frog sartorius and rat extensor digitorum longus muscles was examined. Nicotine (0.005-0.2 mM) did not alter the uptake of ⁴²K in any of the muscles tested. Efflux was significantly increased during the first one to five minutes of nicotine exposure and returned to normal monotonically within an hour in both types of denervated muscle as well as in the innervated frog sartorius muscle. After removal of nicotine, there was a long period (>1.0 hour) during which ⁴²K efflux was decreased 20 to 50% below control values. The time course of ⁴²K efflux stimulation paralleled the time course of muscle cell membrane depolarization. Both the nicotine-induced depolarization and stimulation of ⁴²K efflux were blocked by prior administration of d-tubocurarine and, therefore, were probably initiated by an interaction of nicotine with chemosensitive sites on the muscle cells. The decreased rate of ⁴²K efflux after nicotine removal was not blocked when d-tubocurarine was added immediately after exposure to nicotine. Conduction in sartorius muscle cells was not blocked by low concentrations of nicotine (<0.06 mM) and action potentials recorded during the peak of depolarization were followed by a "late positive afterpotential" of long duration (>150 msec). The magnitude of the late positive afterpotential was increased by reducing the potassium concentration of the bathing medium.