In:
Journal of Applied Physiology, American Physiological Society, Vol. 93, No. 5 ( 2002-11-01), p. 1660-1668
Abstract:
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 Ca 2+ transient, and the L-type Ca 2+ current ( I Ca,L ) in single rat ventricular myocytes. The anion channel blockers 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) and niflumic acid reversibly inhibited the Ca 2+ 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 Ca 2+ concentration but significantly inhibited I Ca,L . In contrast, replacement of extracellular Cl − with the permeant anions NO[Formula: see text], SCN − , and Br − supported the ECC and I Ca,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 I Ca,L , whereas hypertonic stress depressed the contraction and I Ca,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 Ca 2+ channel activity.
Type of Medium:
Online Resource
ISSN:
8750-7587
,
1522-1601
DOI:
10.1152/japplphysiol.00220.2002
Language:
English
Publisher:
American Physiological Society
Publication Date:
2002
detail.hit.zdb_id:
1404365-8
SSG:
12
SSG:
31
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