earticle

영어

It is well documented that the inherent ability of small arteries and arte-rioles to regulate intraluminal diameter in response to alterations in in-travascular pressure determines peripheral vascular resistance and blood flow (termed myogenic response or pressure-induced vasocon-striction/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 intra-cellular signals for the contractility of VSMCs. Although the roles of transient receptor potential (TRP) channels in pressure-induced vaso-constriction are not fully understood to date, TRP channels that are di-rectly activated by mechanical stimuli (e.g., stretch of VSMCs) or indi-rectly 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 re-view 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.