Barry W H, Bridge J H
Division of Cardiology, University of Utah School of Medicine, Salt Lake City.
Circulation. 1993 Jun;87(6):1806-15. doi: 10.1161/01.cir.87.6.1806.
Calcium homeostasis in cardiac myocytes results from the integrated function of transsarcolemmal Ca2+ influx and efflux pathways modulated by membrane potential and from intracellular Ca2+ uptake and release caused predominantly by SR function. These processes can be importantly altered in different disease states as well as by pharmacological agents, and the resulting changes in systolic and diastolic [Ca2+]i can cause clinically significant alterations in contraction and relaxation of the heart. It may be anticipated that a rapid increase in our understanding of the pathophysiology of Ca2+ homeostasis in cardiac myocytes will be forthcoming as the powerful new tools of molecular and structural biology are used to investigate the regulation of Ca2+ transport systems.
心肌细胞中的钙稳态源于跨肌膜Ca2+内流和外流途径的综合功能,这些途径受膜电位调节,也源于主要由肌浆网(SR)功能引起的细胞内Ca2+摄取和释放。在不同疾病状态以及药理制剂作用下,这些过程可能会发生重要改变,由此导致的收缩期和舒张期细胞内Ca2+浓度([Ca2+]i)变化可引起心脏收缩和舒张的临床显著改变。随着分子生物学和结构生物学的强大新工具被用于研究Ca2+转运系统的调节,预计我们对心肌细胞钙稳态病理生理学的理解将迅速增加。