The role of hyperpolarization in the relaxation of smooth muscle of monkey coronary artery.

In monkey coronary arteries, outer and inner muscle had a similar resting potential (-39.5 and -40.0 mV). Both showed strong outward-going rectification, with no regenerative depolarization, on injection of depolarizing current. The depolarization spread electrotonically in all directions, particularly around the vessel wall. Hyperpolarization up to -45 mV by injection of constant current caused relaxation. Depolarization caused contraction. Pulses of field stimulation caused a brief depolarization which was reduced by tetrodotoxin or by stripping of the adventitia. They also caused a prolonged hyperpolarization which was not prevented by either, but was prevented by rubbing of the endothelium. The hyperpolarization in response to field stimulation therefore appears to result from electrically stimulated release of a substance from endothelial cells. Relaxation accompanied this hyperpolarization. It was twice the size of the relaxation produced by a similar hyperpolarization due to constant injection. Isoprenaline also produced hyperpolarization, and relaxation five times that seen with a similar hyperpolarization induced by direct current. Hyperpolarization appears to be an important, but not the only, mediator of relaxation induced in this artery both by endothelial cells and by beta-adrenergic stimulation.