Calcium signalling during excitation-contraction coupling in mammalian atrial myocytes

被引:116
作者
Bootman, Martin D. [1 ]
Higazi, Daniel R.
Coombes, Stephen
Roderick, H. Llewelyn
机构
[1] Babraham Inst, Mol Signalling Lab, Cambridge CB2 4AT, England
[2] Univ Nottingham, Dept Math Sci, Nottingham NG7 2RD, England
[3] Univ Cambridge, Dept Pharmacol, Cambridge CB2 1QJ, England
基金
英国工程与自然科学研究理事会; 英国生物技术与生命科学研究理事会;
关键词
atrial myocytes; Ca2+ signalling; EC coupling; T-tubules;
D O I
10.1242/jcs.03223
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Atrial cardiomyocytes make an important contribution to the refilling of ventricles with blood, which enhances the subsequent ejection of blood from the heart. The dependence of cardiac function on the contribution of atria becomes increasingly important with age and exercise. We know much less about the calcium signals that link electrical depolarisation to contraction within atrial myocytes in comparison with ventricular myocytes. Nevertheless, recent work has shed new light on calcium signalling in atrial cells. At an ultrastructural level, atrial and ventricular myocytes have many similarities. However, a few key structural differences, in particular the lack of transverse tubules (`T-tubules') in atrial myocytes, make these two cell types display vastly different calcium patterns in response to depolarisation. The lack of T-tubules in atrial myocytes means that depolarisation provokes calcium signals that largely originate around the periphery of the cells. To engage the contractile machinery, the calcium signal must propagate centripetally deeper into the cells. This inward movement of calcium is ultimately controlled by hormones that can promote or decrease calcium release within the myocytes. Enhanced centripetal movement of calcium in atrial myocytes leads to increased contraction and a more substantial contribution to blood pumping. The calcium signalling paradigm within atrial cells applies to other cardiac cell types that also do not express T-tubules, such as neonatal ventricular myocytes, and Purkinje cells that aid in the spread of electrical depolarisation. Furthermore, during heart failure ventricular myocytes progressively lose their regular T-tubule expression, and their pattern of response resembles that of atrial cells.
引用
收藏
页码:3915 / 3925
页数:11
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