Role of vascular potassium channels in the regulation of renal hemodynamics

Abstract

K+conductance is a major determinant of membrane potential ( Vm) in vascular smooth muscle (VSMC) and endothelial cells (EC). The vascular tone is controlled by Vmthrough the action of voltage-operated Ca2+channels (VOCC) in VSMC. Increased K+conductance leads to hyperpolarization and vasodilation, while inactivation of K+channels causes depolarization and vasoconstriction. K+channels in EC indirectly participate in the control of vascular tone by several mechanisms, e.g., release of nitric oxide and endothelium-derived hyperpolarizing factor. In the kidney, a change in the activity of one or more classes of K+channels will lead to a change in hemodynamic resistance and therefore of renal blood flow and glomerular filtration pressure. Through these effects, the activity of renal vascular K+channels influences renal salt and water excretion, fluid homeostasis, and ultimately blood pressure. Four main classes of K+channels [calcium activated (KCa), inward rectifier (Kir), voltage activated (KV), and ATP sensitive (KATP)] are found in the renal vasculature. Several in vitro experiments have suggested a role for individual classes of K+channels in the regulation of renal vascular function. Results from in vivo experiments are sparse. We discuss the role of the different classes of renal vascular K+channels and their possible role in the integrated function of the renal microvasculature. Since several pathological conditions, among them hypertension, are associated with alterations in K+channel function, the role of renal vascular K+channels in the control of salt and water excretion deserves attention.