Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME), a nitric oxide synthase inhibitor, causes a reduction of nitric oxide production and results in systemic vasoconstriction1. Rats treated with L-NAME develop high blood pressure associated with vascular remodelling2. Asiatic acid is a triterpenoid component isolated from Centella asiatica. Previous study, we showed the antihypertensive effect of asiatic acid in L-NAME-induced hypertension3. This study was to investigate the effect of asiatic acid on vascular remodelling in L-NAME-induced hypertensive rats. Male Sprague-Dawley rats were treated with L-NAME (40 mg/kg/day) for 3 weeks to induce hypertension. Hypertensive rats were orally administered asiatic acid (20 mg/kg/day) or vehicle for a further two weeks (n = 10/group). Systolic blood pressure (SBP) was measured once a month. At the end of treatment, rats were anaesthetized with peritoneal injection of pentobarbital-sodium (60 mg/kg). Blood samples were collected for measurement plasma tumor necrosis factor-alpha (TNF-α), nitric oxide metabolites (NOx), and malondialdehyde (MDA) levels. Then, rats were sacrificed by overdose of anesthetic drug. The thoracic aorta was isolated to examine vascular remodelling, endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) expression, and MDA levels. All procedures are complied with the standards for the care and use of experimental animals and approved by Animal Ethics Committee of Khon Kaen University, Thailand. Data are expressed as the mean ± S.E.M., compared by ANOVA. We found that hypertensive rats had high SBP compared to that of in control rats (216.8 ± 3.4 vs. 121.4 ± 2.4 mmHg; p < 0.001). There were increases in aortic wall thickness and aortic collagen deposition in hypertensive rats (p < 0.05). Decreased plasma NOx and increased plasma TNF-α were observed in hypertensive rats (p < 0.05); these were consistent with downregulation of eNOS expression and upregulation of iNOS expression in aortic tissues (p < 0.05). MDA levels in plasma and aortic tissues were significantly increased in hypertensive rats (p < 0.05). Asiatic acid markedly reduced SBP (167.5 ± 2.5 mmHg; p < 0.01), alleviated vascular remodelling in hypertensive rats (p < 0.05) comparing to those of untreated rats (p < 0.05). Furthermore, plasma NOx, TNF-α and MDA levels as well as protein eNOS/iNOS expression were improved in the treated group (p < 0.05). In conclusion, this study demonstrates the therapeutic effects of asiatic acid on blood pressure and vascular remodelling, which is possibly related to the restoration of protein eNOS/iNOS expression, and the resulting anti-inflammatory and antioxidant activities.