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Diabetes-induced coronary vascular dysfunction involves increased arginase activity.

Maritza J Romero1, Daniel H Platt, Huda E Tawfik

  • 1Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta, GA 30912, USA.

Circulation Research
|October 31, 2007
PubMed
Summary
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Increased arginase activity in diabetes impairs blood vessel function by reducing nitric oxide (NO) availability. Treatments like simvastatin and L-citrulline show promise in restoring vascular health.

Area of Science:

  • Biochemistry
  • Physiology
  • Pathology

Background:

  • Arginase activity increases in diseases with vascular dysfunction.
  • Arginase competes with nitric oxide synthase (NOS) for L-arginine, a key substrate.

Purpose of the Study:

  • To investigate the role of arginase in diabetes-induced vascular endothelial dysfunction.
  • To determine if increased arginase activity contributes to reduced nitric oxide (NO) production.

Main Methods:

  • Experiments using streptozotocin-induced diabetic rats and high glucose (HG)-treated bovine coronary endothelial cells (BCECs).
  • Assessed vasorelaxation, reactive oxygen species (ROS), arginase activity, arginase I expression, and NO production.
  • Utilized treatments including simvastatin, L-citrulline, arginase inhibitors, and small interfering RNA (siRNA) for arginase I.

Related Experiment Videos

Main Results:

  • Diabetes led to impaired vasorelaxation, increased ROS, arginase activity, and arginase I expression in diabetic rat tissues.
  • HG-treated BCECs showed increased arginase activity, elevated superoxide and RhoA levels, and diminished NO production.
  • Simvastatin, L-citrulline, and arginase inhibition improved vasodilation in diabetic models.
  • Silencing arginase I in BCECs normalized NO production under HG conditions.

Conclusions:

  • Increased arginase activity in diabetes contributes to vascular endothelial dysfunction.
  • This dysfunction is mediated by decreased L-arginine availability for NO synthase.
  • Arginase I plays a significant role in HG-induced reduction of NO production.