Electrical responses of smooth muscle cells of the mouse uterus to adenosine triphosphate.

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.