Abstract
In the cardiac dyad, sarcolemmal L-type Ca(2+) channels (LCCs) and
sarcoplasmic reticulum (SR) Ca(2+) release channels (RyR) are structurally
in close proximity. This organization provides for an efficient functional
coupling, tuning SR Ca(2+) release for optimal contraction of the
myocyte. Given that LCC are regulated by the prevailing Ca(2+),
this structural organization is the setting for feedback mechanisms
and crosstalk. A defective coupling of Ca(2+) influx via LCC to activation
of RyR has been implicated in reduced SR Ca(2+) release in heart
failure. Both functional changes in LCC properties and structural
re-organization of LCC in T-tubules could be involved. LCC are regulated
by cytosolic Ca(2+), and crosstalk with SR Ca(2+) handling occurs
on a long-term basis, i.e. during steady-state changes in heart rate,
on an intermediate-term basis, i.e. on a beat-to-beat basis during
sudden rate changes, and on a very short- or immediate-term basis,
i.e. during a single heartbeat. We review the properties and consequences
of these different feedback mechanisms and the changes in heart failure
and cardiac hypertrophy that have thus far been studied.
- animals;
- arrhythmias,
- biochemical;
- calcium
- calcium,
- cardiac,
- cardiomegaly,
- channel,
- channels,
- contraction;
- etiology;
- failure,
- feedback,
- heart
- humans;
- l-type,
- metabolism;
- myocardial
- physiology
- physiology;
- rate;
- receptor
- release
- reticulum,
- ryanodine
- sarcoplasmic
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