Centre for Vision and Vascular Science, School of Medicine, Dentistry and Biomedical Sciences, Royal Victoria Hospital, Queen's University of Belfast, Belfast BT12 6BA, UK.
Adv Exp Med Biol. 2011;704:707-29. doi: 10.1007/978-94-007-0265-3_37.
Recent studies show that mammalian melastatin TRPM nonselective cation channels (TRPM1-8), members of the largest and most diverse TRP subfamily, are widely expressed in the endothelium and vascular smooth muscles. When activated, these channels similarly to other TRPs permit the entry of sodium, calcium and magnesium, thus causing membrane depolarisation. Although membrane depolarisation reduces the driving force for calcium entry via TRPMs as well as other pathways for calcium entry, in smooth muscle myocytes expressing voltage-gated Ca(2+) channels the predominant functional effect is an increase in intracellular Ca(2+) concentration and myocyte contraction. This review focuses on several best documented aspects of vascular functions of TRPMs, including the role of TRPM2 in oxidant stress, regulation of endothelial permeability and cell death, the connection between TRPM4 and myogenic response, significance of TRPM7 for magnesium homeostasis, vessel injury and hypertension, and emerging evidence that the cold and menthol receptor TRPM8 is involved in the regulation of vascular tone.
最近的研究表明，哺乳动物黑色素瘤相关钙通道 TRPM 非选择性阳离子通道（TRPM1-8）是 TRP 亚家族中最大和最多样化的成员之一，广泛表达于内皮细胞和血管平滑肌中。当这些通道被激活时，它们与其他 TRP 通道一样允许钠离子、钙离子和镁离子进入，从而导致膜去极化。尽管膜去极化会降低通过 TRPM 以及其他钙通道进入的驱动力，但在表达电压门控钙 (Ca2+) 通道的平滑肌细胞中，主要的功能效应是增加细胞内 Ca2+浓度和肌细胞收缩。这篇综述重点介绍了 TRPM 在血管功能方面的几个有充分文献记录的方面，包括 TRPM2 在氧化应激中的作用、内皮通透性和细胞死亡的调节、TRPM4 与肌原性反应的联系、TRPM7 对镁稳态的重要性、血管损伤和高血压以及新兴证据表明冷和薄荷醇受体 TRPM8 参与血管张力的调节。
