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Cardiovascular Research 1993 27(10):1826-1830; doi:10.1093/cvr/27.10.1826
© 1993 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

The relative contributions of different intracellular and sarcolemmal systems to relaxation in rat ventricular myocytes

N Negretti, S C O'Neill and D A Eisner

Department of Veterinary Preclinical Sciences, University of Liverpool, PO Box 147, Liverpool L69 3BX, United Kingdom: N Negretti, S C O'Neill, D A Eisner.

Correspondence to Professor Eisner.

Objective: The aim was to estimate the relative contributions of the various intracellular and sarcolemmal systems to the relaxation of the systolic calcium transient. Methods: The experiments were performed on isolated rat ventricular myocytes. The cells were loaded with the fluorescent indicator indo-1 in order to measure [Ca2+]i. Results: The application of caffeine to release calcium from the sarcoplasmic reticulum produced a rise of [Ca2]i which decayed about 7-8 times more slowly than the electrically stimulated calcium transient. This suggests that the sarcoplasmic reticulum accounts for about 87% of the calcium removal. The rate of decay of the caffeine response was decreased to about 33% of the control by inhibiting the Na-Ca exchange with Ni2+. In the presence of Ni2+ the rate could be inhibited further by inhibiting either the sarcolemmal Ca-ATPase (by increasing extracellular calcium concentration, [Ca2+]o) or the mitochondria (with FCCP and oligomycin). The relative contributions of the various processes were estimated to be: sarcoplasmic reticulum 87%, mitochondria 1.7%, Na-Ca 8.7%, sarcolemmal Ca-ATPase 2.6%. Conclusions: These experiments show that the Na-Ca exchange accounts for 67% of the calcium removal not mediated by the sarcoplasmic reticulum. This is a smaller fraction than in rabbit cardiac cells and highlights the importance of the Ca-ATPase in the rat heart.

Cardiovascular Research 1993;27;1826-1830

KEYWORDS calcium; contraction; Na-Ca


The work described in this paper was supported by grants from the British Heart Foundation and the Wellcome Trust. NN was supported by the Universidad Central de Venezuela.


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