In the present study, we found that Ang II elevated blood pressure significantly, attenuated ACh-induced vascular relaxation, and induced the constriction of the MA, CA, and PA in SHR, which were inhibited by pretreatment with the AT1 receptor antagonist losartan, suggesting the worse effects of activity of the Ang II/AT1 receptor on endothelial dysfunction and hypertension. The gene discussed is AGT; the disease is endothelial dysfunction.