Vascular Physiology Research Group, Department of Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA.
J Cardiovasc Pharmacol. 2011 Feb;57(2):148-53. doi: 10.1097/FJC.0b013e3181f580d9.
Intracellular Ca(2+) plays a dual role in the regulation of vascular tone. Smooth muscle cell Ca(2+) influx causes vasoconstriction, whereas transient localized Ca(2+) release from intracellular stores in either endothelial or vascular smooth muscle cells can elicit membrane hyperpolarization and vasodilation by stimulating Ca(2+)-activated K(+) (K(Ca)) channels. Recent evidence suggests that Ca(2+) influx via transient receptor potential (TRP) channels can cause arterial dilation by activating K(Ca) channels. Current findings in this area are summarized. Key features of the main KCa channels present in the vascular wall (K(Ca)1.1, K(Ca)2.3, and K(Ca)3.1) and TRP channels are briefly reviewed. Arterial dilation mediated by endothelial TRP channels sensitive to dietary molecules are reviewed. Recent reports demonstrate that 2 chemosensitive TRP channels, TRPA1 and TRPV3, are present in native cerebral artery endothelial cells. These channels are activated by substances found in foods such as garlic, mustard oil, and oregano and mediate K(Ca)-dependent endothelium-dependent vasodilation. The role of TRPV4 channels in mediating vasodilation in response to epoxyeicosatrienoic acids (EETs) is also reviewed. Stimulation of TRPV4 channels with 11,12-EET in cerebral artery smooth muscle cells causes membrane hyperpolarization and vasodilation by increasing the frequency of Ca(2+) release from intracellular stores, which in turn increases K(Ca)1.1 channel activity. Evidence that K(Ca)2.3 and K(Ca)3.1 channels in endothelial cells and K(Ca)1.1 channels in smooth muscle are involved in TRPV4-dependent 11,12-EET–induced dilation of mesenteric arteries is discussed. These examples show that Ca(2+) influx through TRP channels in endothelial or smooth muscle cells influences vascular tone by increasing K(Ca) channel activity.
细胞内 Ca(2+) 在血管张力调节中发挥双重作用。平滑肌细胞 Ca(2+) 内流引起血管收缩，而内皮细胞或血管平滑肌细胞内的细胞内储存的短暂局部 Ca(2+) 释放可以通过刺激 Ca(2+)-激活的 K(+) (K(Ca)) 通道引起膜超极化和血管舒张。最近的证据表明，通过瞬时受体电位 (TRP) 通道的 Ca(2+) 内流可以通过激活 K(Ca) 通道引起动脉扩张。本文总结了这一领域的最新发现。简要回顾了血管壁中存在的主要 KCa 通道 (K(Ca)1.1、K(Ca)2.3 和 K(Ca)3.1) 和 TRP 通道的主要特征。审查了对饮食分子敏感的内皮 TRP 通道介导的动脉扩张。最近的报告表明，2 种化学敏感的 TRP 通道，TRPA1 和 TRPV3，存在于天然脑动脉内皮细胞中。这些通道被食物中的物质激活，如大蒜、芥末油和牛至，介导 K(Ca) 依赖性内皮依赖性血管舒张。还审查了 TRPV4 通道在介导对环氧二十碳三烯酸 (EETs) 的血管舒张中的作用。用 11,12-EET 刺激脑动脉平滑肌细胞中的 TRPV4 通道会通过增加细胞内储存的 Ca(2+) 释放频率引起膜超极化和血管舒张，从而增加 K(Ca)1.1 通道的活性。讨论了内皮细胞中的 K(Ca)2.3 和 K(Ca)3.1 通道以及平滑肌中的 K(Ca)1.1 通道在内皮细胞中涉及 TRPV4 依赖性 11,12-EET 诱导的肠系膜动脉扩张的证据。这些例子表明，内皮细胞或平滑肌细胞中通过 TRP 通道的 Ca(2+) 内流通过增加 K(Ca) 通道的活性来影响血管张力。
