Vascular potassium channels in NVC.

It has long been proposed that the external potassium ion ([K+](0)) works as a potent vasodilator in the dynamic regulation of local cerebral blood flow. Astrocytes may play a central role for producing K+ outflow possibly through calcium-activated potassium channels on the end feet, responding to a rise in the intracellular Ca2+ concentration, which might well reflect local neuronal activity. A mild elevation of [K+](0) in the end feet/vascular smooth muscle space could activate Na+/K+-ATPase concomitant with inwardly rectifying potassium (Kir) channels in vascular smooth muscle cells, leading to a hyperpolarization of vascular smooth muscle and relaxation of smooth muscle actin-positive vessels. Also proposed notion is endothelial calcium-activated potassium channels and/or inwardly rectifying potassium channel-mediated hyperpolarization of vascular smooth muscle. A larger elevation of [K+](0), which may occur pathophysiologically in such as spreading depression or stroke, can trigger a depolarization of vascular smooth muscle cells and vasoconstriction instead.