title: Vascular potassium channels in NVC.
abstract: 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 Ca(2+) 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.
authors.affiliation: Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan. Electronic address: kyamada@hirosaki-u.ac.jp.
authors.forename: K
authors.initials: K
authors.lastname: Yamada
mesh_terms: D000818:Animals; D002560:Cerebrovascular Circulation / Q000502:physiology; D008954:Models, Biological; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D011188:Potassium / Q000378:metabolism*; D015221:Potassium Channels / Q000502:physiology*
chemical_list: D015221:Potassium Channels; D011188:Potassium
keywords: Astrocyte; BK channel; Cerebral blood flow; Functional hyperemia; Inward rectifier; KATP channel; Neurovascular coupling; Smooth muscle cell