Vascular physiology of a Ca2+ mobilizing second messenger - cyclic ADP-ribose.
Vascular physiology of a Ca2+ mobilizing second messenger - cyclic ADP-ribose.
复制标题
DOI：
10.1111/j.1582-4934.2006.tb00408.x
复制
发表时间：
2006-04
影响因子：
5.3
通讯作者：
Li PL
中科院分区：
文献类型：
--
作者：
Zhang AY;Li PL
环adp核糖（cADPR）是一种新的Ca2+动员第二信使，它能够通过激活血管细胞中的ryanodine受体（RyR）诱导肌浆网（SR）释放Ca2+。据报道，这种信号核苷酸也参与血管平滑肌细胞（VSMCs）中细胞内Ca2+火花2+波或振荡、Ca2+诱导的Ca2+释放（CICR）和自发瞬时外向电流（STOCs）的产生或调节。关于cADPR介导的信号在介导血管对不同刺激的反应中的作用，越来越多的证据表明，cADPR在血管内皮细胞（ECs）和VSMCs对各种化学因子（如血管活性激动剂乙酰胆碱、氧化摩尔碱、内皮素）和物理刺激（如拉伸、电去极化和绝对应激）的Ca2+反应中起重要作用。这种cadpr - ryr介导的Ca2+信号现在被认为是调节血管功能的基本机制。在这里，我们回顾了有关血管细胞中cADPR信号通路的文献，主要关注cADPR的产生及其在控制血管张力和血管舒缩反应中的生理作用。我们还总结了一些已发表的结果，揭示了介导cADPR在血管细胞中的作用的潜在机制。鉴于Ca2+在血管功能调节中的重要性，本文综述的结果将为血管生理学和循环调节提供新的见解。
Cyclic ADP-ribose (cADPR) is a novel Ca2+ mobilizing second messenger, which is capable of inducing Ca2+ release from the sarcoplasmic reticulum (SR) via activation of ryanodine receptors (RyR) in vascular cells. This signaling nucleotide has also been reported to participate in generation or modulation of intracellular Ca2+ sparks 2+waves or oscillations, Ca2+-induced Ca2+ release (CICR) and spontaneous transient outward currents (STOCs) in vascular smooth muscle cells (VSMCs). With respect to the role of cADPR-mediated signaling in mediation of vascular responses to different stimuli, there is accumulating evidence showing that cADPR is importantly involved in the Ca2+ response of vascular endothelial cells (ECs) and VSMCs to various chemical factors such as vasoactive agonists acetylcholine, oxotemorine, endothelin, and physical stimuli such as stretch, electrical depolarization and sheer stress. This cADPR-RyR-mediated Ca2+ signaling is now recognized as a fundamental mechanism regulating vascular function. Here we reviewed the literature regarding this cADPR signaling pathway in vascular cells with a major focus on the production of cADPR and its physiological roles in the control of vascular tone and vasomotor response. We also summarized some publish results that unveil the underlying mechanisms mediating the actions of cADPR in vascular cells. Given the importance of Ca2+ in the regulation of vascular function, the results summarized in this brief review will provide new insights into vascular physiology and circulatory regulation.