The Ca(2+)-ATPase of the sarcoplasmic reticulum in skeletal and cardiac muscle. An overview from the very beginning to more recent prospects.
The discovery of the ATP-driven calcium pump in the sarcoplasmic reticulum membranes reaches back to the postwar (World War II) years and would not be possible without the generous support by the American scientific community. It was this community that in pre- and postwar years gave shelter to many European scientists, which in return stimulated scientific development in the United States. These pre- and postwar relations helped to establish the calcium pump as a physiologically relevant mechanism in all kinds of cells. The pump and its counterpart, the calcium release channel, proved to be controlled by various intrinsic mechanisms. Rising hydrogen concentrations as occurring in ischemic muscles switch off pump activity and counteract allosterically caffeine-induced calcium release (CICR). Rising phosphate or the presence of other calcium-precipitating anions, on the other hand, prevents pump inhibition by intraluminal calcium precipitation, which, simultaneously, can increase the quantity of releasable calcium. The inactivation of CICR by removing medium chloride must be considered as a hint of additional mechanisms by which calcium-dependent activity regulation can be modified.
Hasselbach
W
W
Max-Planck-Institut für Medizinische Forschung Heidelberg, Germany.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D000252:Calcium-Transporting ATPases / Q000378:metabolism*; D006321:Heart / Q000502:physiology / Q000503:physiopathology; D006801:Humans; D018482:Muscle, Skeletal / Q000201:enzymology*; D017202:Myocardial Ischemia / Q000201:enzymology / Q000503:physiopathology; D009206:Myocardium / Q000201:enzymology*; D012519:Sarcoplasmic Reticulum / Q000201:enzymology* / Q000502:physiology
D000252:Calcium-Transporting ATPases; D002118:Calcium