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Endothelial hypoxic preconditioning in rat hypoxic isolated aortic segments.

Carolina Carrasco-Martín1, Sergio Alonso-Orgaz, Juan C De la Pinta

  • 1Digestive Research Laboratory, Fundación Jiménez Díaz, Hospital Clínico San Carlos, C/Profesor Martín Lagos s/n, Madrid 28040, Spain.

Experimental Physiology
|March 17, 2005
PubMed
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Hypoxic preconditioning enhances endothelial function and nitric oxide synthase levels after hypoxia-reperfusion injury. This protective effect persists even when heat shock protein 90 is inhibited, suggesting other mechanisms are involved.

Area of Science:

  • Cardiovascular Physiology
  • Endothelial Biology
  • Cellular Adaptation

Background:

  • Hypoxia-reperfusion (HR) injury impairs endothelial function.
  • Endothelial hypoxic preconditioning may offer protection against HR injury.
  • Mechanisms underlying endothelial adaptation to HR remain incompletely understood.

Purpose of the Study:

  • To analyze endothelial hypoxic preconditioning following hypoxia-reperfusion (HR).
  • To investigate the impact of hypoxic preconditioning on endothelial function and nitric oxide synthase (eNOS) phosphorylation.
  • To explore the role of heat shock protein 90 (hsp90) in endothelial adaptation to HR.

Main Methods:

  • Isolated rat aortic segments were subjected to hypoxia-reperfusion (HR) with or without prior hypoxic preconditioning (P + HR).

Related Experiment Videos

  • Endothelial function was assessed via acetylcholine (Ach)-induced vasorelaxation.
  • Levels of serine1177 phosphorylated endothelial nitric oxide synthase (ser1177-eNOS) were measured by Western blot.
  • Superoxide anion and peroxynitrite levels were quantified using confocal microscopy.
  • The effect of geldanamycin (hsp90 inhibitor) on ser1177-eNOS and preconditioning was evaluated.

    • Main Results:

    • HR significantly reduced Ach-dependent vasorelaxation, an effect improved by hypoxic preconditioning (P + HR).
    • Hypoxic preconditioning increased ser1177-eNOS levels compared to HR alone.
    • HR led to increased superoxide anion and peroxynitrite, which were reduced by preconditioning.
    • Geldanamycin decreased ser1177-eNOS in P + HR segments, but endothelial protection persisted.

    Conclusions:

    • Short-term hypoxia induces endothelial hypoxic preconditioning, enhancing vascular wall ser1177-eNOS levels.
    • Endothelial hypoxic preconditioning improves endothelial function and reduces oxidative stress after HR injury.
    • The persistence of preconditioning despite hsp90 inhibition suggests alternative molecular pathways mediate endothelial adaptation to HR injury.