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Hypoxia Sensing In The Fetal Chicken Femoral Artery Is Mediated By The Mitochondrial Electron Transport Chain

Bea Zoer, Angel L. Cogolludo, Francisco Perez-Vizcaino, Jo G. R. De Mey, Carlos E. Blanco, Eduardo Villamor

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Vascular hypoxia sensing is transduced into vasoconstriction in the pulmonary circulation, whereas systemic arteries dilate. Mitochondrial electron transport chain (mETC), reactive O2species (ROS), and K+channels have been implicated in the sensing/signaling mechanisms of hypoxic relaxation in mammalian systemic arteries. We aimed to investigate their putative roles in hypoxia-induced relaxation in fetal chicken (19 days of incubation) femoral arteries mounted in a wire myograph. Acute hypoxia (Po2∼2.5 kPa) relaxed the contraction induced by norepinephrine (1 μM). Hypoxia-induced relaxation was abolished or significantly reduced by the mETC inhibitors rotenone (complex I), myxothiazol and antimycin A (complex III), and NaN3(complex IV). The complex II inhibitor 3-nitroproprionic acid enhanced the hypoxic relaxation. In contrast, the relaxations mediated by acetylcholine, sodium nitroprusside, or forskolin were not affected by the mETC blockers. Hypoxia induced a slight increase in ROS production (as measured by 2,7-dichlorofluorescein-fluorescence), but hypoxia-induced relaxation was not affected by scavenging of superoxide (polyethylene glycol-superoxide dismutase) or H2O2(polyethylene glycol-catalase) or by NADPH-oxidase inhibition (apocynin). Also, the K+channel inhibitors tetraethylammonium (nonselective), diphenyl phosphine oxide-1 (voltage-gated K+channel 1.5), glibenclamide (ATP-sensitive K+channel), iberiotoxin (large-conductance Ca2+-activated K+channel), and BaCl2(inward-rectifying K+channel), as well as ouabain (Na+-K+-ATPase inhibitor) did not affect hypoxia-induced relaxation. The relaxation was enhanced in the presence of the voltage-gated K+channel blocker 4-aminopyridine. In conclusion, our experiments suggest that the mETC plays a critical role in O2sensing in fetal chicken femoral arteries. In contrast, hypoxia-induced relaxation appears not to be mediated by ROS or K+channels.