title: Role of vascular potassium channels in the regulation of renal hemodynamics.
abstract: K(+) conductance is a major determinant of membrane potential (V(m)) in vascular smooth muscle (VSMC) and endothelial cells (EC). The vascular tone is controlled by V(m) through the action of voltage-operated Ca(2+) 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 (K(Ca)), inward rectifier (K(ir)), voltage activated (K(V)), and ATP sensitive (K(ATP))] 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.
authors.affiliation: Univ. of Copenhagen, Dept. of Biomedical Sciences, The Panum Institute, Copenhagen, Denmark. cmehlin@sund.ku.dk
authors.forename: Charlotte Mehlin
authors.initials: CM
authors.lastname: Sorensen
authors.forename: Thomas Hartig
authors.initials: TH
authors.lastname: Braunstein
authors.forename: Niels-Henrik
authors.initials: NH
authors.lastname: Holstein-Rathlou
authors.forename: Max
authors.initials: M
authors.lastname: Salomonsson
mesh_terms: D000818:Animals; D004730:Endothelium, Vascular / Q000502:physiology*; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D006978:Hypertension, Renovascular / Q000503:physiopathology; D007668:Kidney / Q000098:blood supply* / Q000503:physiopathology; D015221:Potassium Channels / Q000502:physiology*
chemical_list: D015221:Potassium Channels