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Magnesium modulates endothelial dysfunction produced by elevated glucose incubation

M Félétou1, C Rasetti, J Duhault

  • 1Institut de Recherches Servier, Suresnes, France.

Journal of Cardiovascular Pharmacology
|September 1, 1994
PubMed
Summary
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Low magnesium levels worsen high glucose-induced impairments in rabbit aorta relaxation. Indomethacin partially restored acetylcholine responses in elevated glucose, suggesting prostaglandin involvement in this vascular dysfunction.

Area of Science:

  • Vascular Physiology
  • Endocrinology
  • Pharmacology

Background:

  • Elevated glucose impairs endothelium-dependent relaxation in rabbit aorta.
  • Magnesium ion concentration affects vascular smooth muscle contractility and mediator release.

Purpose of the Study:

  • To investigate the impact of altered magnesium ion concentration on high glucose-induced endothelial dysfunction in isolated rabbit aorta.
  • To explore the role of prostaglandins in these responses.

Main Methods:

  • Ex vivo study of isolated rabbit aorta from normal and diabetic rabbits.
  • Vessels were precontracted with phenylephrine and exposed to varying glucose and magnesium concentrations.
  • Acetylcholine (ACh) and sodium nitroprusside (SNP) were used to assess relaxation and contraction.

Related Experiment Videos

  • Indomethacin was used to inhibit prostaglandin synthesis.

    • Main Results:

    • In 0.6 mM magnesium, elevated glucose (44 mM) impaired endothelium-dependent relaxation to ACh.
    • Indomethacin partially restored ACh-induced relaxation in elevated glucose conditions.
    • Elevated glucose and low magnesium potentiated endothelium-dependent contractions to ACh, abolished by indomethacin.

    Conclusions:

    • Low magnesium exacerbates high glucose-induced endothelial dysfunction in rabbit aorta.
    • Prostaglandins play a significant role in the impaired relaxation and altered contraction observed under these conditions.