Objective: The aims of this study were to search for the role of glucose in the regulation blood pressure of rats and to investigate the effects of glucose on the production of vascular aldosterone and corticosterone in rats. Methods: Male Wistar rats received glucose 15.0 g· kg<sup>–1</sup>·d<sup>–1</sup> (glucose-treated group 1) or 25.0 g·kg<sup>–1</sup>·d<sup>–1</sup> (glucose-treated group 2) or 35.0 g·kg<sup>–1</sup>·d<sup>–1</sup> (glucose-treated group 3), orally, for 3 months, and blood pressure was monitored by a pressure transducer. Mesenteric artery perfusion ex vivo was performed and pressor responses to norepinephrine were determined in Wistar rats. The perfusate from the mesenteric arteries was collected and applied to a Sep-Pak C 18 cartridge column for reverse phase high-performance liquid chromatography and levels of both aldosterone and corticosterone were determined by radioimmunoassay. Reverse transcriptase ploymerase chain reaction was used to measure the expression of 11β-HSD2 and CYP11B2 mRNA in mesenteric arteries. Results: Blood pressure increased in Wistar rats treated with glucose compared to control rats. The pressor responses to norepinephrine in mesenteric arteries treated with glucose were significantly increased. Levels of aldosterone were decreased but those of corticosterone increased in the perfusate from arteries treated with glucose. Reverse transcriptase ploymerase chain reaction showed that glucose inhibited the expression of 11β-HSD2 and CYP11B2 mRNA in mesenteric arteries. Conclusion: These results reveal that glucose able to induce hypertension and provide evidence that glucose inhibits the transcriptions of both 11β-HSD2 and CYP 11B2 in vasculature, leading to lower aldosterone and higher corticosterone production in vessels, and increased vasoconstrictor responses to norepinephrine.