Trafford Andrew W, Díaz M E, O'Neill S C, Eisner D A
Unit of Cardiac Physiology, The University of Manchester, 1.524 Stopford Building, Oxford Rd, Manchester M13 9PT, UK.
Front Biosci. 2002 Apr 1;7:d843-52. doi: 10.2741/trafford.
This review discusses the control of the amplitude of the cardiac systolic Ca transient. The Ca transient arises largely from release from the sarcoplasmic reticulum (SR). Release is triggered by calcium-induced calcium release (CICR) whereby the entry of a small amount of Ca on the L-type Ca current, "the trigger", results in the release of much more Ca from the SR. There are three potential control points: (1) the Ca content of the SR; (2) the properties of the SR Ca release channel or ryanodine receptor (RyR); (3) the amplitude of the L-type Ca current. The data reviewed show that the Ca content of the SR has pronounced effects on systolic [Ca2+]i and, reciprocally, the amount of Ca released from the SR affects sarcolemmal Ca fluxes thereby "autoregulating" SR content. Modulation of the ryanodine receptor has no steady-state effect due to compensating changes of SR Ca content. An increase of the L-type Ca current results in an abrupt increase of systolic [Ca2+]i with little change of SR content. This is because of a coordinated increase of both the trigger and loading function of the Ca current. These results emphasise the importance of considering all aspects of Ca handling in the context of SR Ca release and thus the regulation of the systolic Ca transient and contraction in cardiac muscle.
本综述讨论了心脏收缩期钙瞬变幅度的调控。钙瞬变主要源于肌浆网（SR）的钙释放。钙释放由钙诱导的钙释放（CICR）触发，即少量钙通过L型钙电流进入（“触发”），导致更多的钙从SR释放。存在三个潜在的控制点：（1）SR的钙含量；（2）SR钙释放通道或兰尼碱受体（RyR）的特性；（3）L型钙电流的幅度。所综述的数据表明，SR的钙含量对收缩期[Ca2+]i有显著影响，反之，从SR释放的钙量影响肌膜钙通量，从而“自动调节”SR含量。由于SR钙含量的补偿性变化，兰尼碱受体的调节没有稳态效应。L型钙电流增加导致收缩期[Ca2+]i突然增加，而SR含量变化很小。这是因为钙电流的触发和负载功能同时协调增加。这些结果强调了在SR钙释放的背景下考虑钙处理各个方面的重要性，从而强调了对心肌收缩期钙瞬变和收缩的调节。
