Objective: Endothelium-dependent vasodilatation is impaired in hypertension. Statins have been shown to improve endothelial functions in hyperlipidemic subjects. We aimed to investigate the effect of statins on endothelium-dependent flow mediated dilatation (FMD) and blood pressure (BP) in normocholesterolemic hypertensive patients. Methods: This randomized prospective study consisted of 56 patients with newly diagnosed essential hypertension. All patients received angiotensin converting enzyme (ACE) inhibitor lisinopril (5 mg/day) as antihypertensive therapy, and half of them were randomized to simvastatin(20mg/day) irrespective of serum lipid levels. All subjects underwent brachial artery ultrasonographic examination for the measurement of FMD before randomization and at the end of 12 weeks treatment. Results: A total of 39 patients completed the study (21 patients in the statin + ACE inhibitor group, and 18 patients in the ACE-inhibitor alone group). Blood pressure levels were substantially reduced in both groups after treatment. In statin+ ACE-inhibitor group systolic pressure reduced by 23% (p=0.0001) and diastolic BP reduced by 23% (p=0.0001). In ACE-inhibitor alone group these ratios were 20% (p=0.001) and 21% (p=0.001), respectively. Meanwhile, pulse pressure (PP) decreased by 25% in statin+ ACE-inhibitor group (P=0.0001) and by 16% in ACE inhibitor-alone group (p=0.0051). Baseline FMD was significantly impaired in overall patients with hypertension as compared with healthy controls (13 ± 8 vs. 24±8 %, P = 0.001). After treatment FMD decreased by 23% in lisinopril alone group (p=0.054). There were no correlations between FMD improvement, LDL reduction, BP or PP changes in both groups. Conclusion: Addition of simvastatin to ACE-inhibitor treatment in newly diagnosed hypertensive patients with normal cholesterol levels, significantly reduced PP and facilitated BP control, but did not affect endothelium-dependent dilatation. Further long-term large scale studies are needed to clarify the effect of various statins on endothelial functions of either hypercholesterolemic or normocholesterolemic hypertensive patients.