Intracellular pH regulation in heart

被引:242
作者
Vaughan-Jones, Richard D. [1 ]
Spitzer, Kenneth W. [2 ]
Swietach, Pawel [1 ]
机构
[1] Burdon Sanderson Cardiac Sci Ctr, Dept Physiol Anat & Genet, Oxford OX1 3PT, England
[2] Univ Utah, NE Harrison Cardiovasc Res & Training Inst, Salt Lake City, UT 84112 USA
基金
英国医学研究理事会; 美国国家卫生研究院;
关键词
Cardiac; Heart; Myocyte; pH(i); NHE; NBC; CHE; CBE; H+; OH-; HCO3-; Arrhythmia; Contraction; Cardioprotection; RAT VENTRICULAR MYOCYTES; CARBONIC-ANHYDRASE-II; NA+/H+ EXCHANGER NHE1; SODIUM-HYDROGEN-EXCHANGE; NH2-TERMINAL CYTOPLASMIC DOMAIN; CARDIAC PURKINJE-FIBERS; H+-ION MOBILITY; ELECTROGENIC NA+-HCO3-COTRANSPORT; ACTIVATED PROTEIN-KINASE; SLOW FORCE RESPONSE;
D O I
10.1016/j.yjmcc.2008.10.024
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Intracellular pH (pH(i)) is an important modulator of cardiac excitation and contraction, and a potent trigger of electrical arrhythmia. This review outlines the intracellular and membrane mechanisms that control pHi in the cardiac myocyte. We consider the kinetic regulation of sarcolemmal H+, OH- and HCO3- transporters by pH, and by receptor-coupled intracellular signalling systems. We also consider how activity of these pH(i) effector proteins is coordinated spatially in the myocardium by intracellular mobile buffer shuttles, gap junctional channels and carbonic anhydrase enzymes. Finally, we review the impact of pH(i) regulatory proteins on intracellular Ca2+ signalling, and their participation in clinical disorders such as myocardial ischaemia, maladaptive hypertrophy and heart failure. Such multiple effects emphasise the fundamental role that pHi regulation plays in the heart (C) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码:318 / 331
页数:14
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