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Diversity in mitochondrial function explains differences in vascular oxygen sensing.

Evangelos D Michelakis1, Vaclav Hampl, Ali Nsair

  • 1Department of Medicine (Cardiology) and the Vascular Biology Group, University of Alberta, Edmonton, Alberta, Canada. emichela@cha.ab.ca

Circulation Research
|June 29, 2002
PubMed
Summary
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Mitochondria in pulmonary and renal arteries differ, explaining their opposite responses to low oxygen. This difference in vascular smooth muscle cell mitochondria involves activated oxygen species and K+ channels.

Area of Science:

  • Cardiovascular Physiology
  • Mitochondrial Biology
  • Vascular Physiology

Background:

  • Pulmonary arteries (PAs) constrict, while renal arteries (RAs) dilate in response to hypoxia.
  • Oxygen sensing in PAs involves a redox sensor affecting smooth muscle cell (SMC) function.
  • Mitochondria are candidate vascular oxygen sensors, regulating cellular redox status and potentially K+ channel activity.

Purpose of the Study:

  • To investigate if mitochondrial diversity between vascular beds explains the opposing hypoxic responses of PAs and RAs.
  • To determine the role of mitochondria-derived activated oxygen species (AOS) in regulating vascular tone.

Main Methods:

  • Compared effects of hypoxia and proximal electron transport chain (pETC) inhibitors (rotenone, antimycin A) on rat isolated arteries, SMCs, and perfused organs.

Related Experiment Videos

  • Measured AOS and H2O2 production, outward K+ current, and SMC mitochondrial membrane potential.
  • Assessed expression of pETC components and mitochondrial manganese superoxide dismutase.

    • Main Results:

    • Hypoxia and pETC inhibitors decreased AOS production and outward K+ current, constricting PAs, while increasing AOS and K+ current, dilating RAs.
    • Lung mitochondria exhibited lower respiratory rates and higher basal AOS/H2O2 production compared to RAs.
    • PA rings showed greater AOS/H2O2 production and more depolarized SMC mitochondrial membrane potential than RA rings.

    Conclusions:

    • Pulmonary arteries and renal arteries possess distinct mitochondria.
    • Differential regulation of mitochondria-derived factors, potentially H2O2, explains the opposing vascular responses to hypoxia.
    • Mitochondrial differences in AOS production and K+ channel regulation are key to differential vascular tone.