Department of Surgery, The Chinese University of Hong Kong, Hong Kong.
J Cardiovasc Pharmacol. 2012 Feb;59(2):109-15. doi: 10.1097/FJC.0b013e318210fb4b.
Based on the genetic relationship, single-channel conductance, and gating mechanisms, calcium-activated potassium (KCa) channels identified in vasculature can be divided into 3 groups including large-conductance KCa, small, and intermediate conductance KCa. KCa channels in smooth muscle and endothelial cells are essential for the regulation of vascular tone. Vascular dysfunction under ischemia-reperfusion (I-R) or hypoxia-reoxygenation (H-R) conditions is associated with modulations of KCa channels that are attributable to multiple mechanisms. Most studies in this regard relied on the change of relaxation components sensitive to certain channel blockers to indicate the alteration of KCa channels under I-R conditions, which however provided conflicting results for the effect of I-R. The possible mechanisms involved in KCa channel modulation under I-R/H-R include overproduction of reactive oxygen species such as superoxide anion, hydrogen peroxide, and peroxynitrite, increase of intracellular H ion, and lactate accumulation, etc. However, more studies are necessary to further understand the discrepancies in the sensitivity of KCa channels to I-R injury in different vascular beds.
基于遗传关系、单通道电导和门控机制，在血管中鉴定出的钙激活钾 (KCa) 通道可分为 3 组，包括大电导 KCa、小电导和中电导 KCa。平滑肌和内皮细胞中的 KCa 通道对于调节血管张力至关重要。在缺血再灌注 (I-R) 或缺氧复氧 (H-R) 条件下的血管功能障碍与 KCa 通道的调制有关，这归因于多种机制。在这方面的大多数研究依赖于对某些通道阻滞剂敏感的松弛成分的变化来表示 I-R 条件下 KCa 通道的改变，但对于 I-R 的作用提供了相互矛盾的结果。I-R/H-R 下 KCa 通道调节涉及的可能机制包括活性氧如超氧阴离子、过氧化氢和过氧亚硝酸盐的过度产生、细胞内 H 离子的增加和乳酸的积累等。然而，需要更多的研究来进一步了解不同血管床中 KCa 通道对 I-R 损伤的敏感性差异的机制。
