Motivation: Statins are widely used in the treatment of dyslipidemia, which is usually associated with cardiovascular abnormalities including hypertension. Microvascular rarefaction and endothelial dysfunction are aggravating factors of hypertensive end-organ damage. Thus, this study was designed to investigate the acute effects of simvastatin (SIM) on cerebral microcirculation and endothelial function in spontaneously hypertensive rats (SHR). Methods: Male Wistar normotensive rats (WKY) and SHR were divided into 3 groups of 8 animals each: WKY-CTL and SHR-CTL treated with 0.9% saline solution, and SHR+SIM treated with SIM 30 mg/kg/day during 3 days by gavage. Systolic blood pressure (SBP) was measured by a tail-cuff plethysmography system. Rats were anaesthetised with (50 mg/kg sodium pentobarbital, i.p.). We investigated brain functional capillary density (FCD) and vascular reactivity using intravital fluorescence videomicroscopy after IV injection of FITC labeled dextran. We assessed pial arterioles endothelium-dependent vasodilation responses to acetylcholine (Ach,1µM) administration. Vascular responses were expressed as percentage changes from the baseline arteriolar diameters. Values are means ±S.E.M, compared by ANOVA and Bonferroni’s Test, p values <0.05 were considered significant. All protocols were approved in accordance with the internationally accepted principles for the Care and Use of Laboratory Animals (license # L-48/12). Results: SIM administration reduced SBP in SHR (SHR-CTL 203±3 vs.SHR+SIM 172±6 mmHg;p<0.001). Cerebral FCD was reduced in hypertensive rats compared with normotensive rats (SHR-CTL 337±61 vs. WKY-CTL 421±35 capillaries/mm²;p<0.05). The administration of SIM during 3 days induced a significant increase in cerebral FCD in hypertensive rats (SHR+SIM 530±31 capillaries/ mm²;p<0.05). Ach induced arteriolar vasodilation in WKY rats (WKY-CTL +6.6±1.2%) but arteriolar vasoconstriction in SHR (SHR-CTL -1.4±1.3 %;p<0.05); SIM restored Ach-induced arteriolar vasodilation (SHR+SIM +11.5±3.1%;p< 0.05). Microvascular endothelial dysfunction in SHR was associated with a down-regulation of endothelial nitric oxide synthase (eNOS) expression in the brain (SHR-CTL 0.76±0.1 vs. WKY-CTL1.25±0.2 eNOS/GAPDH (AU);p<0.05). Treatment of SHR with SIM normalized the brain expression of eNOS (SHR+SIM 2.13±0.7 eNOS/GAPDH (AU);p< 0.05). Conclusion: Acute treatment with simvastatin reversed cerebral microvascular rarefaction and restored brain microvascular endothelial function of hypertensive rats. In addition to cholesterol-lowering effects, vascular pleiotropic effects of statins could turn out to be a new therapeutic approach for improving microcirculatory function in hypertensive patients.