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Hyperuricemia induces endothelial dysfunction.

Uday M Khosla1, Sergey Zharikov, Jennifer L Finch

  • 1Baylor College of Medicine, Department of Medicine, Division of Nephrology, Houston, Texas 77030, USA. ukhosla@tmh.tmc.edu

Kidney International
|April 21, 2005
PubMed
Summary
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High uric acid levels impair nitric oxide production, leading to endothelial dysfunction. Lowering uric acid in hyperuricemic rats reversed this impairment, suggesting a mechanism for uric acid-induced vascular disease.

Area of Science:

  • Biochemistry
  • Cardiovascular Physiology
  • Renal Physiology

Background:

  • Hyperuricemia is associated with cardiovascular and renal diseases, potentially via reactive oxygen species (ROS) and endothelial dysfunction.
  • Xanthine oxidase produces ROS and uric acid; allopurinol inhibits this enzyme, reversing endothelial dysfunction.
  • L-arginine supplementation in rats partially reversed hyperuricemia-induced hypertension and vascular disease.

Purpose of the Study:

  • To investigate the hypothesis that uric acid inhibits nitric oxide (NO) production, causing endothelial dysfunction.
  • To determine the effect of hyperuricemia and its reversal on NO levels in rats.
  • To assess the direct impact of uric acid on NO generation in endothelial cells.

Main Methods:

  • Male Sprague-Dawley rats were induced with hyperuricemia using oxonic acid; controls received vehicle.

Related Experiment Videos

  • Allopurinol was administered to inhibit hyperuricemia. Rats were grouped into control, allopurinol only, oxonic acid only, and oxonic acid + allopurinol.
  • Serum uric acid, nitrites/nitrates (NOx), and systolic blood pressure were analyzed. In vitro studies used bovine aortic endothelial cells.

    • Main Results:

    • Oxonic acid induced hyperuricemia; allopurinol reversed it. Hyperuricemic rats showed reduced serum NOx levels, which allopurinol partially or fully reversed.
    • A direct linear correlation was observed between serum uric acid and NOx levels.
    • Uric acid inhibited both basal and VEGF-induced nitric oxide production in cultured endothelial cells.

    Conclusions:

    • Hyperuricemia in rats is characterized by decreased serum nitric oxide, which is restored by lowering uric acid levels.
    • Soluble uric acid directly impairs nitric oxide generation in endothelial cells.
    • Hyperuricemia contributes to endothelial dysfunction, potentially explaining its role in hypertension and vascular disease pathogenesis.