Abstract
The possible contribution of Na(+)-Ca(2+) exchange to the triggering
of Ca(2+) release from the sarcoplasmic reticulum in ventricular
cells remains unresolved. To gain insight into this issue, we measured
the "trigger flux" of Ca(2+) crossing the cell membrane in rabbit
ventricular myocytes with Ca(2+) release disabled pharmacologically.
Under conditions that promote Ca(2+) entry via Na(+)-Ca(2+) exchange,
internal Na(+) (10 mM), and positive membrane potential, the Ca(2+)
trigger flux (measured using a fluorescent Ca(2+) indicator) was
much greater than the Ca(2+) flux through the L-type Ca(2+) channel,
indicating a significant contribution from Na(+)-Ca(2+) exchange
to the trigger flux. The difference between total trigger flux and
flux through L-type Ca(2+) channels was assessed by whole-cell patch-clamp
recordings of Ca(2+) current and complementary experiments in which
internal Na(+) was reduced. However, Ca(2+) entry via Na(+)-Ca(2+)
exchange measured in the absence of L-type Ca(2+) current was considerably
smaller than the amount inferred from the trigger flux measurements.
From these results, we surmise that openings of L-type Ca(2+) channels
increase Ca(2+) near Na(+)-Ca(2+) exchanger molecules and activate
this protein. These results help to resolve seemingly contradictory
results obtained previously and have implications for our understanding
of the triggering of Ca(2+) release in heart cells under various
conditions.
- animals;
- calcium
- calcium,
- cardiac;
- cells,
- channel
- channels,
- cultured;
- cytology;
- exchanger,
- function
- gating,
- heart
- ion
- l-type,
- metabolism;
- myocytes,
- physiology;
- rabbits;
- reticulum,
- sarcoplasmic
- signaling,
- sodium,
- sodium-calcium
- ventricles,
- ventricular
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