Abstract
This review discusses the control of the amplitude of the cardiac
systolic Ca transient. The Ca transient arises largely from release
from the sarcoplasmic reticulum (SR). Release is triggered by calcium-induced
calcium release (CICR) whereby the entry of a small amount of Ca
on the L-type Ca current, "the trigger", results in the release of
much more Ca from the SR. There are three potential control points:
(1) the Ca content of the SR; (2) the properties of the SR Ca release
channel or ryanodine receptor (RyR); (3) the amplitude of the L-type
Ca current. The data reviewed show that the Ca content of the SR
has pronounced effects on systolic Ca$^2+$i and, reciprocally,
the amount of Ca released from the SR affects sarcolemmal Ca fluxes
thereby äutoregulating" SR content. Modulation of the ryanodine
receptor has no steady-state effect due to compensating changes of
SR Ca content. An increase of the L-type Ca current results in an
abrupt increase of systolic Ca$^2+$i with little change of
SR content. This is because of a coordinated increase of both the
trigger and loading function of the Ca current. These results emphasise
the importance of considering all aspects of Ca handling in the context
of SR Ca release and thus the regulation of the systolic Ca transient
and contraction in cardiac muscle.
- 11897570
- animals,
- atpase,
- biological,
- calcium
- calcium,
- channel,
- channels,
- congestive,
- contraction,
- disease
- failure,
- gov't,
- heart
- humans,
- l-type,
- models,
- myocardial
- myocardium,
- non-u.s.
- phosphorylation,
- progression,
- receptor
- release
- research
- reticulum,
- ryanodine
- sarcoplasmic
- signaling,
- support,
- {c}a$^{2+}$-transporting
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