Potassium and potassium clouds in endothelium-dependent hyperpolarizations

A small increase in extracellular K+ acts as a local, physiological regulator of blood flow to certain vascular beds. The K+ derives from active tissues such as contracting skeletal muscle and brain and increases blood Supply to these organs by the activation of Na+/K+-ATPases and/or inwardly-rectifying K+ channels oil the Vascular myocytes. K+ liberated from the vascular endothelium also acts as all endothelium-derived hyperpolarizing and relaxing factor within blood vessels. The K+ effluxes from endothelial cell intermediate- and small-conductance, Ca2+-sensitive K+ channels which open in response to stretch and local hormones. In many vessels, endothelium-derived hyperpolarizing factor (EDHF) seems identical to the K+ derived front endothelial cells: it activates Na+/K+-ATPases (particularly those containing alpha2 and alpha3 subunits) and inward rectifiers (particularly Kir-2.1) located on the vascular invocytes. Vasospastic agents generate "potassium clouds" around vascular smooth muscle cells via the efflux of this ion through large conductance, Ca2+-sensitive K+ channels on the myocytes. These potassium clouds call reduce the hyperpolarizing actions of endothelium-derived K+ by effectively saturating the Na+/K+-ATPases and inward rectifiers oil the muscle cells and they may be of clinical significance in vasospastic conditions. (C) 2004 Elsevier Ltd. All rights reserved.