Article,
Integrated Ca$^2+$ management in cardiac myocytes.
Ann. N. Y. Acad. Sci., (May 2004)
DOI: 10.1196/annals.1302.003
Abstract
Cardiac myocyte excitation-contraction coupling is complex. There
are many systems involved that interact to form varied, but well-tuned,
effects that are essential to contractile regulation. Nearly all
of these systems are Ca-dependent, and Ca homeostasis within the
myocyte is carefully controlled. Contractile activation results from
Ca entry via Ca current, and Ca release from the sarcoplasmic reticulum
(SR). Ca extrusion from the cytosol is controlled by Ca transport
by (1) the Na-Ca exchanger, (2) the SR Ca-pump (which is balanced
by a Ca leak out of the SR), and (3) slower systems (including Ca
transport by mitochondria and the sarcolemmal Ca-pump). These systems
interact to regulate the amount of Ca within the cell at rest, most
of which is stored within the SR. The amount of Ca released from
the SR depends nonlinearly upon SR Ca, specifically the free SR
Ca (Ca(SR)). The relationship is particularly steep at high Ca(SR),
where spontaneous release can take place, resulting in electrical
arrhythmias. In many models of heart failure, SR Ca is reduced,
which may cause decreased Ca release and contractile dysfunction.
In summary, the varied processes responsible for Ca regulation within
the myocyte are critical to normal heart function, and disruption
of the normal operation of these proteins can cause widely varied
pathological effects, in large part due to dysfunctional Ca handling.
Tags
- 15201147
- action
- animals,
- calcium
- calcium,
- cardiac,
- cardiovascular,
- cell
- computer
- contraction,
- gov't,
- heart
- humans,
- ion
- membrane
- membrane,
- models,
- myocardial
- myocardium,
- myocytes,
- non-u.s.
- p.h.s.,
- potentials,
- research
- reticulum,
- sarcoplasmic
- signaling,
- simulation,
- support,
- transport,
- u.s.
- ventricles,
