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Glucose levels observed in daily clinical practice induce endothelial dysfunction in the rabbit macro‐ and microcirculation

We investigated whether different concentrations of elevated glucose – corresponding to levels observed in patients with type 2 diabetes under routine care (post‐prandial mean and maximum values) and those used for diagnosing diabetes – induce impairment of vascular reactivity of the macro‐ and microcirculation in non‐diabetic rabbits. Aortic rings and isolated perfused kidneys from normal rabbits were acutely exposed (3 h) to normal (5.5 mm) or high (7–25 mm) d‐glucose concentrations. Vascular reactivity was evaluated with endothelium‐dependent [acetylcholine (ACh) and bradykinin (BK)] and independent [sodium nitroprusside (SNP)] vasodilating agents. Endothelium‐dependent relaxation of the thoracic aorta induced by ACh or BK was significantly attenuated after a 3‐h exposure to high d‐glucose (15–25 mm) but not after corresponding increased osmolarity with mannitol solutions. Relaxation induced by SNP (endothelium‐independent) was not affected by high d‐glucose concentrations. Moreover, endothelium‐dependent but not independent vasodilation of the isolated rabbit kidney was also impaired after 3‐h perfusion with high d‐glucose (11.1–25 mm). Perfusion with mannitol solutions (15–25 mm) partially blunted endothelium‐dependent renal vasodilation. It is concluded that acute hyperglycemia corresponding to post‐prandial levels in patients with type 2 diabetes induces endothelial dysfunction of conduit vessels as well as of the renal circulation of non‐diabetic rabbits.