The sympathetic nervous system exerts a vasoconstrictor influence over peripheral vascular beds that is counter-regulated by local vascular signaling mechanisms (i.e. sympathetic escape, sympatholysis, and myoendothelial feedback). The endothelium has emerged as a primary site for the regulation of sympathetic vasoconstriction through highly specialized cellular connections called myoendothelial projections (MEPs) that facilitate electrical coupling of endothelial and vascular smooth muscle cells. Endothelial derived hyperpolarization (EDH) via activation of IK channels is an important component of MEP-mediated feedback regulation of sympathetic vasoconstriction in animal models. Recent pharmacological data highlight the unique ability of EDH signaling to attenuate sympathetic vasoconstriction in humans.
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