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Aspects of Heart Respiratory Control by the Mitochondrial Isozyme of Creatine Kinase

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Myocardial and Skeletal Muscle Bioenergetics

Abstract

The isolation of intact mitochondria by Claude (1,2), the refinements by Hogeboom et. al (3), and the recognition by Kennedy and Lehninger (4) that these organelles were the site of oxidative phosphorylation heralded the modern era of cellular bioenergetics. Shortly thereafter, Siekevitz and Potter (5) and others (6–10) began to explore the regulation of mitochondrial respiratory rates and oxidative phosphorylation. The reason for this rather extended quest is straightforward. As seen in Fig. 1, when intact mitochondria are incubated in respiratory medium, oxygen is consumed at an endogenous rate termed State IV. With substrate and Pi present, the addition of ADP (phosphate acceptor), even at micromolar concentrations, results in a marked stimulation of respiration to near-maximum velocity called State III. From the view of cellular physiology, neither State IV or State III are relevant, since the normal rate of oxygen consumption by a tissue, e.g. the heart, lies between these two in vitro rates. Only under conditions of extreme stress does heart oxygen consumption ever come close to maximum respiratory rates. Therefore, the biologically important issue is to determine how a cell modulates oxygen consumption and, thus, high-energy phosphate production, at intermediate rates. The achievement of this involves the notion of respiratory control.

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Jacobus, W.E., Vandegaer, K.M., Moreadith, R.W. (1986). Aspects of Heart Respiratory Control by the Mitochondrial Isozyme of Creatine Kinase. In: Brautbar, N. (eds) Myocardial and Skeletal Muscle Bioenergetics. Advances in Experimental Medicine and Biology, vol 194. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5107-8_14

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