[Role of nitric oxide and mitochondrial permeability pore in changes of oxygen consumption in the working skeletal muscle].
On anaesthetized dogs the role NO and mitochondrial permeability transition pore (MPTP) in the regulation of regional blood circulation, efficiency of oxygen using, and muscle contraction force was investigated. Under different frequency stimulation it was shown, that short-term (30") smoothly tetanic contraction (40 Hz) is more economic for a skeletal muscle than short-term (30") single contractions (8 Hz) with respect to the efficiency of oxygen using. Injection NOS inhibitor L-NMMA (2.7 mg/kg, i.a.) resulted in pronounced fall of a functional hyperemia magnitude (P < 0.01), significant reduction of the muscle contractions force (P < 0.01), and efficiency of oxygen using (P < 0.01), in m.gastrocnemicus, in comparison with control. Pretreatment with an exogenous activator of MPTP phenilarsine oxide (PAO, 0.2 mg/kg, i.a.) caused a marked inhibition of an endothelium-dependent vessels dilation on skin-muscle region of rear limb. At the same time the muscle contractions force was significantly decreased (P < 0.01) and efficiency of oxygen using was diminished too (P < 0.01). This was accompanied by an appearance in blood from v. femoralis mitochondrial factor (MF), indicating MPTP activation. Preliminary injection of the exogenous NO donor sodium nitroprusside (0.2 mg/kg, i.v.) prevented considerably an inhibition of a dilation vessels reserve, a fall of muscle contractions force (P < 0.01) and considerably reduced oxygen cost (P < 0.01) of a m.gastercnemicus work also. The concentration of MF in blood from v. femoralis also was considerably reduced (P < 0.001) that has been the evidence of MPTP inhibition. Thus, activation of MPTP and development of oxidative stress resulted in endothelium dysfunction, a force of muscle contraction diminishing and a significant decrease in efficiency of oxygen using. NO essentially reduced the negative effects of MPTP activation and was antagonist of oxidative damages development.
Sahach
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VF
A.A. Bogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, Kiev.
Bohuslavs'kyĭ
A Iu
AIu
Dmytriieva
A V
AV
Nadtochiĭ
S M
SM
D000818:Animals; D001152:Arsenicals / Q000494:pharmacology; D004285:Dogs; D004558:Electric Stimulation; D007473:Ion Channels / Q000378:metabolism / Q000502:physiology*; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology*; D018482:Muscle, Skeletal / Q000098:blood supply / Q000378:metabolism / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D009599:Nitroprusside / Q000494:pharmacology; D010101:Oxygen Consumption / Q000502:physiology*; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D019323:omega-N-Methylarginine / Q000494:pharmacology
D001152:Arsenicals; D007473:Ion Channels; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; C029341:oxophenylarsine; D009599:Nitroprusside; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase