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Endothelial dysfunction in diabetes mellitus

M Chakir1, G E Plante

  • 1Department of Pharmacology, Medical School, University of Sherbrooke, Québec, Canada.

Prostaglandins, Leukotrienes, and Essential Fatty Acids
|January 1, 1996
PubMed
Summary
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Diabetic rats show increased capillary leakage in multiple organs. Aminoguanidine normalized permeability, suggesting nitric oxide involvement, while aldose reductase inhibitors specifically improved kidney function.

Area of Science:

  • Physiology
  • Pharmacology
  • Endocrinology

Background:

  • Diabetes mellitus is associated with microvascular complications, including increased capillary permeability.
  • Endothelial dysfunction plays a critical role in the pathogenesis of diabetic complications.
  • Nitric oxide (NO) and aldose reductase (AR) pathways are implicated in diabetes-related vascular abnormalities.

Purpose of the Study:

  • To investigate the temporal pattern of albumin extravasation in various tissues of streptozotocin-induced diabetic rats.
  • To evaluate the therapeutic effects of aminoguanidine (a NO modulator) and aldose reductase inhibitors (sorbinil, ARI 509) on diabetes-induced capillary leakage.

Main Methods:

  • Albumin extravasation was quantified using the Evan's blue (EB) technique in streptozotocin-induced diabetic rats.

Related Experiment Videos

  • Rats were treated with aminoguanidine or aldose reductase inhibitors.
  • EB leakage was measured in the upper bronchi, heart, kidney, duodenum, pancreas, skeletal muscle, and skin at different time points.

    • Main Results:

    • Early transient decrease in EB leakage in lung, heart, and skeletal muscle was observed.
    • Significant and progressive increase in EB extravasation occurred in skin, duodenum, upper bronchus, pancreas, and kidney over the course of diabetes.
    • Aminoguanidine treatment normalized capillary permeability in most examined tissues.
    • Aldose reductase inhibitors selectively reduced EB extravasation in the kidney.

    Conclusions:

    • Nitric oxide (NO) is implicated in the development of endothelial dysfunction and capillary permeability abnormalities in this model of diabetes.
    • Aldose reductase inhibitors demonstrate tissue-specific efficacy, particularly in normalizing kidney capillary permeability.
    • Targeting NO pathways and aldose reductase may offer therapeutic strategies for managing diabetic microvascular complications.