Intracellular Free Calcium in Hypertrophy and Failure
作者： Judith K. Gwathmey , Ronglih Liao , Roger J. Hajjar
DOI: 10.1007/978-1-4615-2594-3_7
关键词: Homeostasis 、 Calcium in biology 、 Endoplasmic reticulum 、 Muscle hypertrophy 、 Cardiac muscle 、 Chemistry 、 Myofilament 、 Biophysics 、 Calcium 、 Depolarization
摘要: The human heart contracts and relaxes rhythmically while constantly adapting its output to the hemodynamic constraints of body [1]. In working myocardium, contractile mechanism is activated deactivated by rise fall intracellular calcium concentration ([Ca2+]i), which initiated when membrane depolarization allows Ca2+ enter myoplasm trigger release from sarcoplasmic reticulum (SR). This “triggered” binds troponin, resulting in force development. Relaxation occurs as dissociates proteins taken up SR extruded a Ca2+-ATPase pump Na+-Ca2+ exchange. activating released into does not maximally activate myofilaments, thus allowing cardiac muscle have large reserve. For this reason abnormalities [Ca2+]i homeostasis can lead function [2].
springer.com
springerlink.com参考文章(27)
W Grossman, P D Allen, J K Gwathmey, R E Erny, Abnormal intracellular calcium handling, a major cause of systolic and diastolic dysfunction in ventricular myocardium from patients with heart failure. Circulation. ,vol. 81, ,(1990)
R. J. Hajjar, W. Grossman, Judith K. Gwathmey, Responsiveness of the myofilaments to Ca2+ in human heart failure: implications for Ca2+ and force regulation Cellular and Molecular Alterations in the Failing Human Heart. ,vol. 87, pp. 143- 159 ,(1992) , 10.1007/978-3-642-72474-9_12
M.W Roe, J.J Lemasters, B Herman, Assessment of Fura-2 for measurements of cytosolic free calcium Cell Calcium. ,vol. 11, pp. 63- 73 ,(1990) , 10.1016/0143-4160(90)90060-8
D.T. Yue, W.G. Wier, Estimation of intracellular [Ca2+] by nonlinear indicators. A quantitative analysis Biophysical Journal. ,vol. 48, pp. 533- 537 ,(1985) , 10.1016/S0006-3495(85)83810-8
A B Borle, An overview of techniques for the measurement of calcium distribution, calcium fluxes, and cytosolic free calcium in mammalian cells. Environmental Health Perspectives. ,vol. 84, pp. 45- 56 ,(1990) , 10.1289/EHP.908445
D J Beuckelmann, M Näbauer, E Erdmann, Intracellular calcium handling in isolated ventricular myocytes from patients with terminal heart failure. Circulation. ,vol. 85, pp. 1046- 1055 ,(1992) , 10.1161/01.CIR.85.3.1046
R Ventura-Clapier, H Mekhfi, G Vassort, Role of creatine kinase in force development in chemically skinned rat cardiac muscle The Journal of General Physiology. ,vol. 89, pp. 815- 837 ,(1987) , 10.1085/JGP.89.5.815
E Marban, M Kitakaze, Y Koretsune, D T Yue, V P Chacko, M M Pike, Quantification of [Ca2+]i in perfused hearts. Critical evaluation of the 5F-BAPTA and nuclear magnetic resonance method as applied to the study of ischemia and reperfusion. Circulation Research. ,vol. 66, pp. 1255- 1267 ,(1990) , 10.1161/01.RES.66.5.1255
V Schouten, Altered calcium handling at normal contractility in hypertrophied rat heart Journal of Molecular and Cellular Cardiology. ,vol. 22, pp. 987- 998 ,(1990) , 10.1016/0022-2828(90)91038-9
J.K. Gwathmey, R.J. Hajjar, Intracellular calcium related to force development in twitch contraction of mammalian myocardium. Cell Calcium. ,vol. 11, pp. 531- 538 ,(1990) , 10.1016/0143-4160(90)90029-T