Abstract
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.
- 1716049
- amp,
- animals,
- channels,
- chloride
- chlorides,
- cyclic
- electrophysiology,
- female,
- gov't,
- heart,
- ion
- membrane
- non-u.s.
- p.h.s.,
- potentials,
- pregnancy,
- proteins,
- research
- support,
- u.s.
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