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Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
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Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes

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Carvedilol ameliorates endothelial dysfunction in streptozotocin-induced diabetic rats

Guo-Sheng Fu1, He Huang, Fei Chen

  • 1Department of Cardiology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, 3 East Qingchun Road, Hangzhou, 310016, China.

European Journal of Pharmacology
|June 15, 2007
PubMed

Insights

Carvedilol treatment improved blood vessel function in diabetic rats by increasing nitric oxide and enhancing the expression and activity of nitric oxide synthase 3 (NOS3). This suggests carvedilol can combat diabetic endothelial dysfunction.

Area of Science:

  • Pharmacology
  • Cardiovascular Research
  • Diabetology

Background:

  • Carvedilol, a beta-blocker, exhibits endothelium-dependent vasodilating properties.
  • The effect of carvedilol on endothelial function in diabetes and its mechanism remain unclear.
  • Diabetic complications often involve impaired endothelial function.

Purpose of the Study:

  • To investigate carvedilol's effect on aortic endothelial response in a diabetic rat model.
  • To elucidate the underlying mechanism of carvedilol's action on endothelial function in diabetes.

Main Methods:

  • Measurement of acetylcholine-induced relaxation and sodium nitroprusside (SNP)-induced relaxation in rat aortas.
  • Quantification of nitric oxide synthase 3 (NOS3) mRNA and protein expression, and NOS3 phosphorylation.
  • Assessment of serum nitric oxide (NO) levels after 5 weeks of carvedilol administration (1 or 10 mg/kg/day) in diabetic and non-diabetic rats.

Main Results:

  • Diabetic rat aortas showed reduced endothelium-dependent relaxation and lower serum NO levels.
  • Carvedilol treatment prevented the decline in endothelium-dependent relaxation and serum NO levels in diabetic rats.
  • Carvedilol significantly increased NOS3 mRNA expression, protein levels, and Ser1177 phosphorylation in both healthy and diabetic aortas.

Conclusions:

  • Chronic carvedilol administration ameliorates endothelial dysfunction in diabetic rat aortas.
  • Increased nitric oxide levels and up-regulation of NOS3 expression and phosphorylation are key mechanisms involved.
  • Carvedilol shows therapeutic potential for managing diabetic vascular complications.

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