Abstract
It is generally known that mitochondria isolated from a great variety of tissues have the capacity to take up calcium ions efficiently against a concentration gradient (for reviews, see Lehninger et al., 1967; Carafoli, 1973). The transport process receives the necessary energy either directly from coupled electron transport in the respiratory chain, in which case calcium uptake is abolished by respiratory inhibitors but not by oligomycin, or from hydrolysis of adenosine triphosphate (ATP) by the mitochondrial ATPase, in which case transport is unaffected by respiratory chain inhibitors but is inhibited by oligomycin. These relationships are summarized in Fig. 1. The exact nature of the mitochondrial “energy pressure” in equilibrium with the redox reactions of the respiratory chain as well as with the ATP/ADP-Pi system is not known with certainty (for review, see, e.g., Slater, 1971). It has been proposed that mitochondrial calcium transport is catalyzed by a specific carrier situated in the mitochondrial inner membrane. (Lehninger and Carafoli, 1970; Carafoli, 1973). However, the metabolic significance of mitochondrial calcium transport has not been unequivocally established, although it seems evident that it must be involved in the control of the cytoplasmic calcium concentration, a parameter which, in turn, very delicately controls a variety of intracellular activities (see e.g., Rasmussen, 1970).
Supported by the Ford Foundation and the Finnish State Council for Medical Sciences.
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Wikström, M., Ahonen, P., Luukkainen, T. (1974). A Possible Regulatory Role of Mitochondrial Calcium Uptake in Uterine Contractions. In: Coutinho, E.M., Fuchs, F. (eds) Physiology and Genetics of Reproduction. Basic Life Sciences, vol 4. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-2892-6_14
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