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Glucose levels observed in daily clinical practice induce endothelial dysfunction in the rabbit macro‐ and microcirculation
Author(s) -
Gomes Marília B.,
Affonso Felipe S.,
Cailleaux Solange,
Almeida Andressa L. F.,
Pinto Leonardo F. C.,
Tibiriçá Eduardo
Publication year - 2004
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.2004.00248.x
Subject(s) - medicine , endocrinology , vasodilation , microcirculation , sodium nitroprusside , bradykinin , mannitol , perfusion , endothelium , diabetes mellitus , endothelial dysfunction , acetylcholine , chemistry , nitric oxide , biochemistry , receptor
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 m m ) or high (7–25 m m ) 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 m m ) 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 m m ). Perfusion with mannitol solutions (15–25 m m ) 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.