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Relationships Between Mitochondrial Membrane Potential, NAD(P)H Redox, Superoxide and Force Generation in Bovine Coronary Arteries
Author(s) -
Kaminski Pawel M,
Gao Qun,
Gupte Sachin A,
Wolin Michael S
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a724-c
Subject(s) - redox , superoxide , nad+ kinase , chemistry , coronary arteries , mitochondrion , biophysics , cardiology , biochemistry , medicine , biology , artery , inorganic chemistry , enzyme
Recent studies with diazoxide have suggested this mitochondrial potassium channel (Kmit) opener causes increases in mitochondrial superoxide. Thus we compared the actions of diazoxide and the protonophore mitochondrial uncoupler FCCP on NAD(P)H UV autofluoresence and mitochondrial hyperpolarization‐associated JC‐1 red fluorescence, 5 μM lucigenin‐detectable superoxide and force generated by 30 mM KCl in endothelium‐removed bovine coronary arteries. Diazoxide (0.2 mM) and 4 μM FCCP decreased NAD(P)H and JC‐1 fluorescence, without altering force generated by KCl. However, only diazoxide caused detectable increases in superoxide which were not altered by 0.1 mM apocynin an inhibitor of Nox oxidase activation. Smooth muscle cells freshly isolated from BCA showed an increase mitochondrial localized superoxide detected with MitoSOX. Thus, the opening of Kmit with diazoxide, but not changes in mitochondrial membrane potential or NAD(P)H redox is associated with increased mitochondrial superoxide generation, and the ROS produced does not alter KCl‐elicited force generation under these conditions examined. (Supported by NIH grants: HL31069, HL43023, HL66331)