Mechanism of potassium relaxation of arterial muscle

Abstract

Strips of arterial muscle were prepared from rat tail and femoral arteries and dog mesenteric arteries. All muscles developed a contracture slowly when exposed to a potassium-free solution, but relaxed rapidly when potassium was added to the bath to give a concentration as low as 0.1 mM. The slow contracture is caused by norepinephrine release from intrinsic nerve endings, but the rapid relaxation occurs while the norepinephrine concentration is still high. Contractions produced by exogenous norepinephrine or serotonin in a potassium-free bath were also made to relax by the addition of potassium. After several minutes these relaxations reversed abruptly and spontaneously to return to their original level of contraction. The rapid relaxation was found to be due to an electrogenic transport mechanism which caused hyperpolarization within several seconds after the addition of potassium. This hyperpolarization is believed to be caused by electrogenic ion transport since it exceeded the expected membrane potential based on the potential calculated from potassium concentrations, EK. Hyperpolarization declined within 5-15 min, allowing contraction to redevelop. Ouabain was found to prevent both the potassium-induced relaxation and the cessation of norepinephrine release. However, ouabain prevented relaxation as effectively in denervated as in innervated smooth muscle. We conclude that the initial relaxation of arterial smooth muscle that occurs when potassium is reintroduced into a potassium-free solution is caused by membrane hyperpolarization resulting from the enhanced activity of an electrogenic pump; it is not caused by cessation of norepinephrine release.