Potassium dilates rat cerebral arteries by two independent mechanisms.

Cerebral blood flow is regulated by brain metabolism, and there is evidence to suggest that changes in extracellular potassium concentration are important in linking brain metabolic activity with blood supply. In this study, the effect of low concentrations of potassium on the spontaneous tone of resistance-sized isolated posterior cerebral arteries from Wistar-Kyoto rats was examined. At a transmural pressure of approximately 58 mmHg, the vessels developed spontaneous tone that was 69 +/- 2% of their fully relaxed diameter of 184 +/- 2 microns (n = 50). Introduction of potassium (less than 5 mM) after a 5-min period in potassium-free physiological saline solution resulted in transient dilations, which were not attenuated by barium or cesium but abolished by ouabain. However, potassium concentrations between 7 and 15 mM produced dilations that lacked a transient component and were sensitive to barium, cesium, and ouabain. Maintained dilations to 10 mM K+ persisted in tetrodotoxin, tetraethylammonium, and glibenclamide and after endothelium removal. These results suggest that potassium dilation of cerebral arteries has two independent components, the first of which may be caused by stimulation of the electrogenic sodium pump (0-5 mM K+), whereas the second (greater than 7 mM K+) results from activation of a ouabain-, barium-, and cesium-sensitive process. The latter process describes a means by which potassium may effect prolonged changes in cerebral blood flow.