It has been shown previously that high glucose causes direct and acute endothelial dysfunction in non-diabetic isolated rabbit kidney. This study assessed whether exercise training is able to maintain normal renal vascular endothelial function despite high glucose exposure. Animals were pen confined (SED) or treadmill trained over a 12-week period (ExT). Kidneys isolated from SED and ExT rabbits were continuously perfused ex vivo during 3 h with Krebs-Henseleit solutions containing normal (5.5 mm) or high (15 mm) concentrations of d-glucose. In the SED 5.5 group, acetylcholine (ACh) induced dose-related vasodilator responses, reaching the maximum of 41+/- 2% (n=10; P<0.05). In the kidneys perfused with high concentrations of glucose (SED 15), endothelium-dependent vasodilation was significantly blunted. Maximal relaxation in the presence of 15 mm glucose was of 19 +/- 2%, which was significantly different from the SED 5.5 group (41+/- 2%, n=10, P<0.01). In the ExT 5.5 group, ACh-induced vasodilation was significantly enhanced when compared with the SED 5.5 group, reaching the maximum of (52+/- 2%, n=10, P<0.05). Moreover, the exposure of the renal circulation of ExT animals to high glucose did not change endothelium-dependent vasodilation induced by ACh (46+/- 3%, n=6), when compared with the ExT 5.5 group. Finally, exercise training prevented the deleterious effects of high glucose on endothelial-dependent renal vasodilation (SED 15: 19+/- 2% vs. ExT 15: 46+/- 3%; P<0.05). It is concluded that exercise training protects the rabbit renal circulation against endothelial dysfunction elicited by acute exposure to moderately elevated glucose levels, corresponding to the postprandial glycemia of diabetes type 2 patients under treatment. The enhanced renal vasodilator reserve elicited by exercise training turns out to be a response that protects the kidney from the deleterious effects of glycemic peaks.