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1 School of Pharmacy and Biochemistry, University of Buenos Aires, Laboratory of Free Radical Biology, Buenos Aires, Argentina
2 School of Medicine, University of Buenos Aires, Institute for Cardiological Research, Buenos Aires, Argentina
* To whom correspondence should be addressed. E-mail: tamaraz{at}ffyb.uba.ar.
Mitochondrial NO production was assayed in rats submitted to hypobaric hypoxia and in normoxic controls (53.8 and 101.3 kPa air pressure, respectively). Heart mitochondria from young normoxic animals produced 0.62 and 0.37 nmol NO/min.mg protein in metabolic states 4 and 3, respectively. This production accounts for a release to the cytosol of 29 nmol NO/min.g heart and for 55 % of the NO generation. The mitochondrial nitric oxide synthase (mtNOS) activity measured in submitochondrial membranes at pH 7.4 was 0.69 nmol NO/min. mg protein. Rats exposed to hypobaric hypoxia for 2 to 18 mo showed 20-60 % increased left ventricle mtNOS activity as compared with their normoxic siblings. Left ventricle NADH-cytochrome oxidase and cytochrome oxidase activities decreased by 36 % and 12 % from 2 to 18 mo of age, but were not affected by hypoxia. Mitochondrial NOS up-regulation in hypoxia was associated with a retardation of the decline in the mechanical activity of papillary muscle upon aging and an improved recovery after anoxia-reoxygenation. The correlation of left ventricle mtNOS activity with papillary muscle contractility (determined as developed tension, maximal rate of contraction and relaxation) showed an optimal mtNOS activity (0.69 nmol/min.mg protein). Heart mtNOS activity is regulated by O2 in the inspired air and seems to play a role in NO-mediated signaling and myocardial contractility.
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