Fig. 1. Transient receptor potential (TRP) channel-mediated endothelium-dependent hyperpolarization (EDH) and vasodilation. TRP channels (e.g., representatively TRPV4 channels) are placed myoendothelial projections (MEPs) that are extensions of endothelial cells (ECs) through internal elastic lamina to contact adjacent vascular smooth muscle cells (VSMCs). Localized Ca2+ entry through endothelial TRP channels stimulate intermediate/small conductance Ca2+-sensitive potassium (IKCa/SKCa) channels and in turn results in EDH via K+ ion efflux. EDH is transmitted to adjacent VSMCs through myoendothelial gap junctions (MEGJs) comprising of two hemi-channels, which initiates VSMC hyperpolarization. The altered membrane potential of VSMCs suppresses voltage-dependent Ca2+ channels (VDCCs) and evokes vasodilation.
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