Kim Kijeong, Hong Kwang-Seok
School of Exercise & Sport Science, College of Natural Sciences, University of Ulsan, Ulsan, Korea.
Department of Physical Education, College of Education, Chung-Ang University, Seoul, Korea.
J Exerc Rehabil. 2021 Feb 23;17(1):4-10. doi: 10.12965/jer.2040836.418. eCollection 2021 Feb.
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 Ca (e.g., Ca 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.
有充分的文献记载，小动脉和微动脉响应血管内压力变化调节管腔直径的内在能力决定了外周血管阻力和血流量（称为肌源性反应或压力诱导的血管收缩/扩张）。阻力动脉的这种自动调节特性主要源于机械敏感的血管平滑肌细胞（VSMC）。VSMC的质膜中有多种生物装置，可感知机械刺激并产生细胞内信号以调节VSMC的收缩性。尽管瞬时受体电位（TRP）通道在压力诱导的血管收缩中的作用至今尚未完全明确，但由机械刺激直接激活（如VSMC的拉伸）或由细胞内分子间接诱发（如肌醇三磷酸）的TRP通道是Ca的主要来源（如Ca内流或从肌浆网释放），进而引发血管反应性。本综述旨在总结几十年来越来越多的证据，即TRP经典通道、TRP褪黑素通道、TRP香草酸通道和TRP多囊蛋白通道的激活有助于肌源性血管收缩。
