Role of vascular potassium channels in the regulation of renal hemodynamics

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Charlotte Mehlin Sørensen, Thomas Hartig Braunstein, Niels-Henrik von Holstein-Rathlou, Max Salomonsson

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 Vm through 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.

OriginalsprogEngelsk
TidsskriftAmerican Journal of Physiology: Renal Physiology
Vol/bind302
Udgave nummer5
Sider (fra-til)F505-F518
Antal sider14
ISSN1931-857X
DOI
StatusUdgivet - 1 mar. 2012

ID: 38256443