It is well documented that the inherent ability of small arteries and arterioles to regulate intraluminal diameter in response to alterations in intravascular pressure determines peripheral vascular resistance and blood flow (termed myogenic response or pressure-induced vasoconstriction/dilation). This autoregulatory property of resistance arteries is primarily originated from mechanosensitive vascular smooth muscle cells (VSMCs). There are diverse biological apparatuses in the plasma membrane of VSMCs that sense mechanical stimuli and generate intracellular signals for the contractility of VSMCs. Although the roles of transient receptor potential (TRP) channels in pressure-induced vasoconstriction are not fully understood to date, TRP channels that are directly activated by mechanical stimuli (e.g., stretch of VSMCs) or indirectly evoked by intracellular molecules (e.g., inositol trisphosphate) provide the major sources of Ca2+ (e.g., Ca2+ influx or release from the sarcoplasmic reticulum) and in turn, evoke vascular reactivity. This review sought to summarize mounting evidence over several decades that the activation of TRP canonical, TRP melastatin, TRP vanilloid, and TRP polycystin channels contributes to myogenic vasoconstriction.
Keywords: Ion channel; Mechanotransduction; Microcirculation; Pressure-induced vasoconstriction; Vascular smooth muscle cells.
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