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Department of Experimental Cardiology, Masonic Medical Research Laboratory, Utica, New York 13501
The contributions of electrogenic
sodium/calcium exchange current
(INaCa),
calcium-activated chloride conductance
[ICl(Ca)], and calcium-activated nonselective cation conductance to delayed afterdepolarizations (DAD) were examined. Nonselective
cation channels were absent in canine M cells, since inhibition of
INaCa and
ICl(Ca)
eliminated all calcium-activated currents without abolishing cell
shortening. After the cells were treated with isoproterenol and ouabain
to increase calcium loading,
INaCa was 168 ± 30 × 10
3 pC/pF
and ICl(Ca) was
114 ± 24 × 103
pC/pF. Transient overlapping inward and outward currents were evoked
positive to the chloride reversal potential
(ECl). Outward current was chloride sensitive, and inward current was blocked by
replacement of external sodium with lithium. When
ECl was 
50 mV, triggered activity occurred in normal external sodium and persisted
after inhibition of
INaCa. Steps to
80 mV revealed oscillating inward currents in normal sodium and
chloride, which persisted after inhibition of
INaCa. When
ECl was equal to
113 mV,
ICl(Ca) opposed
INaCa at the
resting potential. DAD occurred in normal sodium, and inhibition of
outward ICl(Ca)
provoked triggered activity. We conclude that
INaCa represents
~60% of the total calcium-activated current at resting potentials
but that both INaCa and
ICl(Ca) work in
concert to cause DAD in calcium-overloaded cells.
sodium/calcium exchange; calcium-activated chloride conductance; transient inward current; nonselective cation conductance
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