Abstract
Ca$^2+$i is used as a signal in many tissues. In this review
we discuss the mechanisms that regulate Ca$^2+$i and, importantly,
what determines their stability. Brief mention is made of the effects
of feedback gain and delays on stability. The control of cytoplasmic
Ca concentration is shown to be generally stable as Ca pumping is
essentially an instantaneous function of Ca$^2+$i. In contrast,
regulation of the Ca content of intracellular stores may be less
stable. One example of this is instability in the control of sarcoplasmic
reticulum (SR) Ca content in cardiac muscle. An increase of SR Ca
content increases the systolic Ca transient amplitude. This in turn
decreases Ca influx into the cell and increases efflux, thereby restoring
SR Ca to control levels. This feedback system has an inherent delay
and is potentially unstable if the gain is increased beyond a certain
level. This instability produces Ca transients of alternating amplitude
and may contribute to the clinical syndrome of pulsus alternans.
- 15572459
- adaptation,
- animals,
- arrhythmia,
- calc,
- calcium,
- channel
- channels,
- conduction
- fluid,
- gating,
- heart
- heart,
- humans,
- intracellular
- ion
- ium
- muscle,
- physiological,
- reticulum,
- sarcoplasmic
- skeletal,
- system,
Users
Please
log in to take part in the discussion (add own reviews or comments).