Main systems involved in calcium regulation in cardiac muscle cells and their functional relationship.
This article discusses interrelationship between various transport proteins in the regulation of intracellular calcium ion concentration in heart muscle cells. The depolarization of the plasma membrane of the cardiac muscle cell causes opening of the L-type calcium channels which triggers the opening of ryanodine receptor (RyR) and releases calcium from intracellular store in sarcoplasmic reticulum (SR) by the process of calcium-induced calcium release (CICR). A major factor responsible for the amount of calcium available during systole is loading of SR by SERCA. The amount of calcium released during systolic calcium transient affects the sarcolemmal Ca2+ and Na(+)-Ca2+ exchange currents. These processes control cell Ca2+ loading and amount of Ca2+ available for uptake by SR and for the next contraction. Each system involved in Ca2+ intracellular concentration is also regulated by physiological mediators and pharmacological compounds that can influence the heart muscle performance. A spatial organization of enzymatic and transport proteins that are responsible for a specific rise in local calcium concentration is also discussed.
Wrzosek
A
A
Department of Muscle Biochemistry, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warszawa, Poland.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000502:physiology*; D002352:Carrier Proteins / Q000502:physiology*; D006801:Humans; D016623:Ion Pumps / Q000502:physiology; D008929:Mitochondria, Heart / Q000378:metabolism; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D012519:Sarcoplasmic Reticulum / Q000502:physiology
D015220:Calcium Channels; D002352:Carrier Proteins; D016623:Ion Pumps; D002118:Calcium