Electrophysiological study of the action of angiotensin II on the rat myometrium.

Angiotensin II (A II) produces a contraction of visceral and vascular smooth muscles of different species. The accompanying electrophysiological changes were measured on strips of rat myometrium at 35 degrees C using the double sucrose-gap technique. A II at concentrations from 5 x 10(-10) to 10(-6)M produces a depolarization and an increase in membrane conductance. This increase in membrane conductance is not membrane potential dependent since it is observed even when the membrane potential is maintained at the resting level. When all Na + in the test solution is replaced by either Li + or Mg (2+), the depolarizing effect of 10(-6)M A II is either markedly reduced or abolished. Under these conditions, A II produces a small initial hyperpolarization, which is modified by external potassium concentration changes and abolished by tetraethylammonium chloride. When all Cl- is replaced by either NO (-3) or cyclohexanesulfamate, A II (10(-6) M) still produces a 20-m V depolarization. The removal of extracellular Ca (2+) or K+ does not have any effect on the depolarizing action of A II, which also is not changed by 10(-3) M ouabain. In conclusion, A II produces a depolarization of the uterine smooth muscle membrane through an increase in the membrane conductance to Na+. The membrane conductance to potassium is increased simultaneously. The contraction induced by A II shows two components: a phasic component triggered by the Ca (2+) entry associated with spike production and a tonic component due to the release of Ca(2+) from intracellular stores.