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Indinavir impairs endothelial function in healthy HIV-negative men.

Sudha S Shankar1, Michael P Dubé, J Christopher Gorski

  • 1Division of Endocrinology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA.

American Heart Journal
|November 18, 2005
PubMed
Summary

HIV protease inhibitor indinavir impairs vascular function in healthy males by affecting nitric oxide production and increasing insulin resistance. This study highlights potential risks of antiretroviral therapy on cardiovascular health.

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Area of Science:

  • Cardiovascular Science
  • Pharmacology
  • Endocrinology

Background:

  • Potent antiretroviral therapy (ART) reduces HIV mortality but may accelerate atherosclerosis.
  • Endothelial dysfunction is a potential mechanism linking ART to cardiovascular disease.

Purpose of the Study:

  • To investigate the effects of the HIV-1 protease inhibitor indinavir on vascular function in HIV-negative individuals.
  • To assess indinavir's impact on endothelial nitric oxide production and insulin sensitivity.

Main Methods:

  • Eight HIV-negative healthy males received daily oral indinavir for 4 weeks.
  • Leg blood flow responses to methacholine chloride, sodium nitroprusside, and NG-mono-methyl-L-arginine were measured before and after treatment.
  • Lipids, insulin sensitivity, inflammation, and oxidative stress markers were also assessed.

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Main Results:

  • Indinavir impaired endothelium-dependent vasodilation and nitric oxide-dependent vascular tone.
  • Fasting insulin levels and HOMA-IR scores significantly increased, indicating insulin resistance.
  • No significant changes were observed in blood pressure, lipids, inflammation, or oxidative stress markers.

Conclusions:

  • Four weeks of indinavir induced vascular dysfunction in healthy individuals, primarily affecting endothelial nitric oxide production.
  • This vascular dysfunction may be partly mediated by induced insulin resistance.
  • Further research is needed to explore other potential mechanisms contributing to indinavir-induced vascular dysfunction.