Chloride conductance pathways in heart.
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Am. J. Physiol. 261 (3 Pt 1): C399--C412 (September 1991)

Nonelectrogenic movement of Cl$^-$ is believed to be responsible for the active accumulation of intracellular Cl$^-$ in cardiac muscle. The electro-neutral pathways underlying this nonpassive distribution of Cl$^-$ are believed to include Cl$^-$-HCO3- exchange, Na$^+$-dependent cotransport (operating as Na$^+$-Cl$^-$ and Na$^+$-K$^+$-2Cl$^-$ cotransport), and K$^+$-Cl$^-$ cotransport. The electrogenic movement of Cl$^-$ in cardiac muscle is particularly interesting from a historical perspective. Until recently, there was some doubt as to whether Cl$^-$ carried any current in the heart. Early microelectrode experiments indicated that a Cl$^-$ conductance probably played an important role in regulating action potential duration and resting membrane potential. Subsequent voltage-clamp experiments identified a repolarizing, transient outward current that was believed to be conducted by Cl$^-$, yet further investigation suggested that this transient outward current was more likely a K$^+$ current, not a Cl$^-$ current. This left some doubt as to whether Cl$^-$ played any role in regulating membrane potential in cardiac muscle. More recent studies, however, have identified a highly selective Cl$^-$ conductance that is regulated by intracellular adenosine 3',5'-cyclic monophosphate, and it appears that this Cl$^-$ current may play an important role in the regulation of action potential duration and resting membrane potential.
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