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P. Ghafourifar, C. Richter

Mitochondrial Nitric Oxide Synthase Regulates Mitochondrial Matrix pH

Nitric oxide (nitrogen monoxide, NO) exerts a wide profile of its biological activities via regulation of respiration and respiration-dependent functions. The presence of nitric oxide synthase (NOS) in mitochondria (mtNOS) was recently reported by us (Ghafourifar and Richter, FEBS Lett. 418, 291–296, 1997) and others (Giulivi et al., J. Biol. Chem. 273, 11038–11043, 1998). Here we report that NO, provided by an NO donor as well as by mtNOS stimulation, regulates mitochondrial matrix pH, transmembrane potential and Ca²⁺ buffering capacity. Exogenously-added NO causes a dose-dependent matrix acidification. Also mtNOS stimulation, induced by loading mitochondria with Ca²⁺, causes mitochondrial matrix acidification and a drop in mitochondrial transmembrane potential. Inhibition of mtNOS's basal activity causes mitochondrial matrix alkalinization and provides a resistance to the sudden drop of mitochondrial transmembrane potential induced by mitochondrial Ca²⁺ uptake. We conclude that mtNOS plays a critical role in regulating mitochondrial ?pH.

Biological Chemistry, Walter de Gruyter

Print ISSN: 1431-6730
Volume: 380, 07/1999
Pages: 1025 - 1028

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