Potassium-induced relaxation in isolated cerebral arteries contracted with prostaglandin F2?

Abstract

Summary In helically cut strips of canine cerebral arteries exposed to 5.4 mM [K⁺]_o and contracted with prostaglandin F_2α, the addition of K⁺ in concentrations ranging from 0.5–5 mM caused a dose-related relaxation. The relaxing effect of K⁺ was potentiated at reduced [K⁺]_o and suppressed at reduced [Na⁺]_o. Reduction of Cl⁻ from bathing media failed to alter the effect of K⁺. Removal of external Ca²⁺ markedly attenuated the K⁺-induced relaxation and increase in [Ca²⁺]_o also attenuated the relaxation. Similar relaxation was induced by K⁺ in cerebral arteries from other species including humans, puppies, cats and rabbits. The addition of K⁺ also elicited a relaxation in peripheral arteries, including coronary, femoral, mesenteric and renal, contracted with prostaglandin, but this relaxation was markedly less than in cerebral arteries. The content of Na⁺ in freshly excised cerebral arteries was significantly greater than that of peripheral arteries, while the content of K⁺ in these arteries was not significantly different. The present study provides further evidence to support the hypothesis that an electrogenic Na⁺ pump is involved in the genesis of K⁺-induced relaxation. The Na⁺ pump does not appear to be fully activated at normal [K⁺]_o of 5.4 mM in cerebral arteries.