Journal of Applied Physiology
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J Appl Physiol (August 2, 2002). doi:10.1152/japplphysiol.00220.2002
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Articles in PresS, published online ahead of print August 2, 2002
J Appl Physiol, 10.1152/jap.00220.2002
Submitted on March 14, 2002
Accepted on July 20, 2002

Anion channels influence excitation-contraction coupling by modulating L-type Ca2+ channel in ventricular myocytes

Shi-Sheng Zhou1*, Zhan Gao1, Ling Dong1, Yan-Feng Ding1, Xiao-Dong Zhang1, Yue-Min Wang1, Jian-Ming Pei1, Feng Gao1, and Xin-Liang Ma1

1 Department of Physiology, The Fourth Military Medical University, Xi'an, China

* To whom correspondence should be addressed. E-mail: sszhou{at}webmail.fmmu.edu.cn.

Anion channels are extensively expressed in the heart but their roles in cardiac excitation-contraction coupling (ECC) are poorly understood. We therefore investigated the effects of anion channels on cardiac ventricular ECC. Edge detection, fura 2 fluorescence measurements and whole-cell patch-clamp techniques were used to measure cell shortening, the intracellular Ca2+ transient and the L-type Ca2+ current (ICa,L) in single rat ventricular myocyte. The anion channel blockers, 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) and niflumic acid (NFA), reversibly inhibited the Ca2+ transients and cell shortening in a dose-dependent manner. Comparable results were observed when the majority of the extracellular Cl- was replaced with the relatively impermeant anions, glutamate (Glt-) and aspartate (Asp-). NPPB and NFA or the Cl- substitutes did not affect the resting intracellular Ca2+ concentration ([Ca2+]i), but significantly inhibited ICa,L. In contrast, replacement of extracellular Cl- with the permeant anions, NO3-, SCN- and Br- , supported the ECC and ICa,L,which still were sensitive to NPPB. Exposure of cardiac ventricular myocytes to a hypotonic bath solution enhanced the amplitude of cell shortening and supported ICa,L, whereas hypertonic stress depressed the contraction and ICa,L. Moreover, cardiac contraction was completely abolished by NPPB (50 µM) under hypotonic conditions. It is concluded that a swelling-activated anion channel may be involved in the regulation of cardiac ECC through modulating L-type Ca2+ channel activity.




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