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*

*Corresponding author for this work

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Zoer B, Cogolludo AL, Perez-Vizcaino F, De Mey JG, Blanco CE, Villamor E. Hypoxia sensing in the fetal chicken femoral artery is mediated by the mitochondrial electron transport chain. Am J Physiol Regul Integr Comp Physiol 298: R1026-R1034, 2010. First published January 20, 2010; doi: 10.1152/ajpregu.00500.2009.Vascular hypoxia sensing is transduced into vasoconstriction in the pulmonary circulation, whereas systemic arteries dilate. Mitochondrial electron transport chain (mETC), reactive O-2 species (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 similar to 2.5 kPa) relaxed the contraction induced by norepinephrine (1 mu M). 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 O-2 sensing in fetal chicken femoral arteries. In contrast, hypoxia-induced relaxation appears not to be mediated by ROS or K+ channels.
Original languageEnglish
Pages (from-to)R1026-R1034
JournalAmerican Journal of Physiology-regulatory Integrative and Comparative Physiology
Issue number4
Publication statusPublished - Apr 2010


  • reactive oxygen species
  • potassium channels
  • systemic vascular

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