Abstract
In 12-15-day pregnant rat myometrium, spikes of the longitudinal muscle were discharged spontaneously in bursts, while the circular muscle had predominantly a plateau potential. In the longitudinal muscle, phenylephrine (10-7 g/ml) slightly decreased the duration of the burst discharge and suppressed the contraction by β-adrenoreceptor stimulation. In the circular muscle, phenylephrine (10-7 g/ml) prolonged the duration of the plateau potential leading to an increase in tension without changing the amplitude of plateau, membrane potential and membrane conductance by α-adrenoreceptor stimulation. The effects of phenylephrine on the circular muscle in various ionic environments were observed. In K-free solution, spike generation ceased but phenylephrine depolarized the membrane, generated the prepotential with spikes and prolonged plateau duration. In low-Ca solution, spontaneous spike generation ceased and electrically evoked spikes showed short plateau duration. Phenylephrine restored the membrane activity and prolonged the plateau duration. Excess Ca showed either prolonged (<5 mM) or reduced (>8 mM) the plateau duration, but phenylephrine consistently prolonged plateau duration. When Cl was replaced with either Br or benzene sulphonate, the former prolonged plateau duration and increased the excitability, whereas the latter reduced plateau duration and suppressed the spontaneous activity. Phenylephrine prolonged plateau duration in both Cl-deficient solutions. When NaCl was replaced bycholine-Cl, leaving 15.7 mM Na remaining in NaHCO3 buffer, phenylephrine action completely ceased. The ionic mechanism involved in phenylephrine action is discussed.
