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Graier, WF; Wascher, TC; Lackner, L; Toplak, H; Krejs, GJ; Kukovetz, WR.
Exposure to elevated D-glucose concentrations modulates vascular endothelial cell vasodilatory response.
Diabetes. 1993; 42(10):1497-1505 Doi: 10.2337/diabetes.42.10.1497
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Leading authors Med Uni Graz: Graier Wolfgang
Co-authors Med Uni Graz: Krejs Günter Josef; Toplak Hermann; Wascher Thomas
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Abstract:: The possible role of endothelial dysfunction in early stages of uncomplicated diabetes mellitus was investigated in porcine aortic endothelial cells. Prolonged exposure to various D-glucose concentrations resulted in concentration-dependent amplification of agonist-induced Ca2+ mobilization, whereas L-glucose and D-mannitol failed to mimic the effect of D-glucose. This stimulatory effect of high D-glucose on endothelial Ca2+ mobilization could be antagonized by coincubation with cytochalasin B, which prevented D-glucose uptake into the cells. In agreement with its effect on agonist-induced Ca2+ response, prolonged preincubation with pathological D-glucose concentrations amplified formation of endothelium-derived relaxing factor, which is well established to be strictly attributable to increases in endothelial free Ca2+. In contrast to endothelium-derived relaxing factor formation stimulated by receptor-interacting autacoids, preincubation with high D-glucose failed to modulate A 23,187-induced endothelium-derived relaxing factor formation, which is attributable to unphysiological increases in endothelial free Ca2+ by this ionophore. Similar to its effect on D-glucose-mediated amplification of agonist-stimulated Ca2+ mobilization, cytochalasin B abolished the stimulatory effect of high D-glucose on endothelium-derived relaxing factor formation. We therefore suggest that prolonged exposure to pathological high D-glucose concentrations results in an enhanced endothelium-derived relaxing factor formation caused by amplification of agonist-stimulated Ca2+ mobilization in endothelial cells. This mechanism may be of particular importance representing a possible basis of pathological vasodilation and reduced peripheral resistance in early stages of diabetes mellitus.
Find related publications in this database (using NLM MeSH Indexing): Animals -; Aorta -; Biological Transport -; Bradykinin - pharmacology; Calcimycin - pharmacology; Calcium - analysis Calcium - metabolism; Cells, Cultured -; Cytochalasin B - pharmacology; Dose-Response Relationship, Drug -; Endothelium, Vascular - chemistry Endothelium, Vascular - drug effects; Glucose - pharmacology; Mannitol - pharmacology; Nitric Oxide - pharmacology; Stereoisomerism -; Swine -; Time Factors -; Vasodilation - drug effects