Potassium-induced relaxation in isolated cerebral arteries contracted with prostaglandin F2alpha.

In helically cut strips of canine cerebral arteries exposed to 5.4 mM [K+]o and contracted with prostaglandin F2alpha, the addition of K+ in concentrations ranging from 0.5 - 5 mM caused a dose-related relaxation. The relaxing effect of K+ was potentiated 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.]