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J Appl Physiol 93: 1660-1668, 2002. First published August 2, 2002; doi:10.1152/japplphysiol.00220.2002
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Vol. 93, Issue 5, 1660-1668, November 2002

Anion channels influence ECC by modulating L-type Ca2+ channel in ventricular myocytes

Shi-Sheng Zhou, Zhan Gao, Ling Dong, Yan-Feng Ding, Xiao-Dong Zhang, Yue-Min Wang, Jian-Ming Pei, Feng Gao, and Xin-Liang Ma

Department of Physiology, The Fourth Military Medical University, Xi'an 710032, China

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 myocytes. The anion channel blockers 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) and niflumic acid 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 niflumic acid or the Cl- substitutes did not affect the resting intracellular Ca2+ concentration but significantly inhibited ICa,L. In contrast, replacement of extracellular Cl- with the permeant anions NO<UP><SUB>3</SUB><SUP>−</SUP></UP>, SCN-, and Br- supported the ECC and ICa,L, which were still sensitive to blockade by 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.

swelling-activated chloride channel; anion channel blocker; calcium transient; heart


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