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Electrical responses of the smooth muscle cells to ATP were recorded in the longitudinal muscle of mouse myometrium, using intracellular micro-electrodes. ATP (greater than 10(-7) M) dose-dependently produced a biphasic change in the membrane potential, an initial hyperpolarization (20-30 sec) and then a depolarization. This effect of ATP was observed in all stages of gestation. The initial hyperpolarization was more quickly desensitized than the depolarization. Application of ATP for a short period (10 sec) produced only the initial hyperpolarization; the amplitude was dose-dependently increased. During the ATP-induced hyperpolarization and the depolarization, generation of spike potentials was suppressed and enhanced, respectively. Strong outward current restored the spike generation during hyperpolarization. During the ATP-induced hyperpolarization, the membrane resistance was decreased. The amplitude of the hyperpolarization was increased in low [K]0 solution and decreased in high [K]0 solutions. Pre-treatment with TEA (1 mM), procaine (1 mM), 4-aminopyridine (0.5 mM) or apamin (2 X 10(-7) M) did not, but TEA (5-10 mM) did suppress the ATP-induced hyperpolarization. Involvement of endogenous catecholamines, cyclic AMP, prostaglandins or acetylcholine in the ATP responses was ruled out. During the ATP-induced depolarization, the membrane resistance was reduced. In low [Na]0 solutions, the muscle membrane was depolarized and the amplitude of ATP-induced depolarization was reduced. In sodium-free solution, ATP produced only the initial hyperpolarization. It was concluded that the electrical responses of the smooth muscle cells of mouse myometrium to ATP consist of two components: an initial hyperpolarization with increase in the potassium conductance and a depolarization with increase in the sodium conductance.

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