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Exposure to elevated D-glucose concentrations modulates vascular endothelial cell vasodilatory response
W F Graier1, T C Wascher, L Lackner
1Institute of Pharmacology and Toxicology, University Graz, Austria.
Diabetes
|October 1, 1993
Summary
High blood sugar (D-glucose) in early diabetes mellitus amplifies calcium signals in endothelial cells. This leads to increased endothelium-derived relaxing factor, potentially causing vasodilation.
Area of Science:
- Endocrinology
- Vascular Biology
- Cellular Physiology
Background:
- Endothelial dysfunction is implicated in early diabetes mellitus.
- The precise mechanisms linking hyperglycemia to endothelial dysfunction require further elucidation.
Purpose of the Study:
- To investigate the role of high D-glucose concentrations in endothelial dysfunction.
- To explore the impact of D-glucose on calcium (Ca2+) mobilization and endothelium-derived relaxing factor (EDRF) formation in porcine aortic endothelial cells.
Main Methods:
- Porcine aortic endothelial cells were exposed to varying concentrations of D-glucose, L-glucose, and D-mannitol.
- Agonist-induced Ca2+ mobilization and A23187-induced EDRF formation were measured.
- The effect of cytochalasin B on D-glucose uptake and EDRF formation was assessed.
Main Results:
- Prolonged exposure to high D-glucose amplified agonist-induced Ca2+ mobilization in a concentration-dependent manner.
- High D-glucose enhanced endothelium-derived relaxing factor formation, correlating with Ca2+ mobilization.
- Cytochalasin B blocked D-glucose uptake and abolished the stimulatory effects of high D-glucose on Ca2+ mobilization and EDRF formation.
Conclusions:
- Prolonged exposure to high D-glucose potentiates agonist-stimulated Ca2+ mobilization in endothelial cells.
- This amplification leads to enhanced EDRF formation, suggesting a mechanism for pathological vasodilation in early diabetes mellitus.