OBJECTIVE - The purpose of this study was to test whether a short-course treatment with ACE inhibitors may restore endothelium-dependent and/or -independent vasodilation in the femoral artery of microalbuminuric patients with type 1 diabetes and normal arterial pressure. RESEARCH DESIGN AND METHODS - We studied nine normotensive microalbuminuric type 1 diabetic patients and two groups of control subjects matched for femoral artery diameter to type I diabetic patients after placebo (control group A, n = 17) and ACE inhibitor (control group B, n = 18) treatment, respectively. The patients were enrolled in a double-blind cross-over study with a 1-week trial of either placebo, captopril (25 mg t.i.d.), or enalapril (10 mg/day) in randomized order to ascertain whether short-term ACE inhibition obtained with (captopril) or without (enalapril) a sulfhydryl donor molecule ameliorates Vessel wall function. Endothelium-mediated Row-dependent vasodilation and endothelium-independent vasodilation were evaluated in the right common femoral artery by echo Doppler. RESULTS - Both captopril and enalapril normalized (control group B 22.9 +/- 3.2% per 8 min) endothelium-dependent response (19.6 +/- 7.5 and 18.0 +/- 5.3 vs. -10.4 +/- 4.1% per 8 min, P < 0.01, for both captopril and enalapril versus placebo, respectively) in the type I diabetic patients. Captopril (28.4 +/- 3.5 vs. 17.1 +/- 3.5%, per 5 min during placebo, P < 0.05) but not enalapril (20.1 +/- 3.0 vs. 31.7 +/- 2.8% per 5 min, P < 0.05 for enalapril Versus control group B, and NS for captopril vs. control group B) ameliorated endothelium-independent vasodilation in type 1 diabetic patients. CONCLUSIONS - ACE inhibition improves endothelium-dependent vasodilation in the femoral artery of normotensive microalbuminuric type 1 diabetic patients. Captopril also ameliorates endothelium-independent vasodilation, possibly through its sulfhydryl donor properties. These results may beef pathophysiological relevance to prevent cardiovascular complications in these patients.