The contribution of mitochondrial calcium ion exchange to relaxation of tension in cardiac muscle.
The possible contribution of mitochondrial Ca2+ accumulation and release to contractile phenomena has been investigated. Two intracellular fractions of Ca2+ sequestration can be identified in cardiac myocytes, one ascribed to mitochondria. Two modes of Ca2+ transport exist within the mitochondrial fraction, one dependent upon mitochondrial respiration and the other upon extramitochondrial [Na+]. Experiments with trabeculae show that under appropriate conditions, the rate of relaxation and the amount of tension developed is dependent on these two modes of Ca2+ transport. A model is presented quantifying the contribution of the mitochondria to relaxation.
Fry
C H
CH
Dept of Physiology, St. Thomas' Hospital Medical School (UMDS), London, UK.
Miller
D J
DJ
Harding
D P
DP
Harrison
S M
SM
D000818:Animals; D001693:Biological Transport, Active; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D004072:Digitonin / Q000494:pharmacology; D007474:Ion Exchange; D007700:Kinetics; D008929:Mitochondria, Heart / Q000378:metabolism*; D009126:Muscle Relaxation; D009200:Myocardial Contraction / Q000502:physiology*; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D012503:Saponins / Q000494:pharmacology; D012519:Sarcoplasmic Reticulum / Q000378:metabolism; D012964:Sodium / Q000378:metabolism
D012503:Saponins; D002110:Caffeine; D012964:Sodium; D004072:Digitonin; D002118:Calcium