. The present study investigated the effect of harmine on hypertension, oxidative stress and vascular remodeling induced by cadmium (Cd) in mice. The results demonstrated that harmine treatment of the mice effectively reversed the Cd-induced increase in systolic blood pressure, diastolic blood pressure and mean arterial pressure. Moreover, treatment with harmine inhibited the Cd-induced vascular responsiveness impairment in dose -dependent manner. Treatment of the mice with harmine significantly (p < 0.05) elevated eNOS level and suppressed the expression of iNOS. Harmine treatment of the Cd exposed mice reduced the level of nitrate/nitrite in urine samples and decreased the Cd-induced increase in thickness of thoracic aorta wall. The Cd-induced decrease in ratio of circumferential extension of the mice thoracic aorta was also effectively attenuated on treatment with harmine. Treatment of the Cd-exposed mice with harmine inhibited the increase in level of MMP-2 and MMP-9 in dose -dependent manner. Administration of harmine reversed the Cd-induced increase in production of O2N- and decrease in GSH level in mice. Treatment of the Cd exposed mice with harmine suppressed the increase in MDA level in cardiac and kidney tissues. Harmine treatment also inhibited the Cd-induced increase in level of protein carbonyl in mice plasma in dose -dependent manner. In summary, the present study demonstrates that harmine treatment exhibits protective effect on Cd induced hypertension in mice through regulation of arterial stiffness, vascular remodeling and oxidative response. Therefore, harmine treatment protects against cadmium -induced hypertension in mice model through inhibition of oxidative stress and improvement of vascular remodeling.