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• W2948163984 abstract "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 IKCa 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." @default.
• W2948163984 created "2019-06-14" @default.
• W2948163984 creator A5018876796 @default.
• W2948163984 creator A5084954833 @default.
• W2948163984 date "2019-04-01" @default.
• W2948163984 modified "2023-10-14" @default.
• W2948163984 title "Escape, lysis, and feedback: endothelial modulation of sympathetic vasoconstriction" @default.
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• W2948163984 doi "https://doi.org/10.1016/j.coph.2019.04.002" @default.
• W2948163984 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31170683" @default.
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