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Electrical activity was recorded intracellularly from the uterine longitudinal muscle of estrogen-treated rat. Membrane potential was -59 mV. Action potential consisted of initial spike and the following plateau potential on which repetitive spike discharge rode. Tetracaine (0.1, 0.2 mM) reduced the maximum rates of rise and fall of initial spike and increased the duration of plateau potential. Sustained depolarization at -33 mV was produced by the application of 0.8 mM tetracaine. The membrane depolarization was accompanied with the increase in membrane resistance. Reduction of initial spike by tetracaine in the maximum rates of rise and fall was prevented by increasing the external Ca concentration and accelerated by decreasing it. In low K (1.2 mM) or isoprenaline (10(-8) M)-containing solution, tetracaine-induced prolongation of plateau potential was inhibited. Plateau potential was reduced in amplitude and was prolonged only slightly by tetracaine in low Na solution (sucrose substitution). Both the initial spike and plateau potentials were blocked completely by 0.2 mM tetracaine in the presence of Mn (0.5 mM) or verapamil (0.5 microM). It is speculated that tetracaine suppresses the K conductances responsible for resting membrane potential and the repolarizations of spike and plateau potentials. Ca influx during the generation of action potential is also supposed to be inhibited by tetracaine.

Electrophysiological effects of tetracaine on the longitudinal muscle of rat uterus in various ionic environments.