SummaryTelmisartan is an angiotensin II receptor blocker (ARB) and also an activator of peroxisome proliferator-activated receptor-γ (PPAR-γ). We investigated whether telmisartan improves vascular endothelial function in patients with essential hypertension with the production of endothelial nitric oxide synthase (eNOS) through PPAR-γ.Telmisartan was administered to 15 patients with essential hypertension. To assess vascular function, asymmetric dimethylarginine (ADMA), an eNOS inhibitor synthesized by endothelial cells, and the pulse-wave velocity (PWV) were measured. The serum levels of lipid, glucose, and glycohemoglobin (HbA1c) were also evaluated before and after treatment. Telmisartan therapy significantly decreased the blood pressure and total-and LDL-cholesterol levels. HbA1c was also significantly improved but not in fasting plasma glucose. The serum levels of ADMA were significantly decreased (0.48 ± 0.08 to 0.42 ± 0.05 nmol/mL; P = 0.01). PWV values were significantly decreased by telmisartan from 1,822.5 ± 352.3 to 1,661.5 ± 299.8 cm/second (P = 0.04*). Telmisartan decreased PWV presumably via the activation of PPAR-γ , suggesting that this agent improves vascular endothelial function via its pleiotropic effects, a mechanism that is different from its hypotensive effects. (Int Heart J 2009; 50: 73-83) Key words: Telmisartan, Vascular endothelial function, Essential hypertension, PPAR-γ , ADMA THE impairment of endothelium causes atherosclerosis, 1) and consequently cerebrovascular and cardiovascular accidents, and is related to poor clinical outcome. Nitric oxide (NO) is a potent vasodilator produced by nitric oxide synthase (NOS) in endothelium, and controls vascular function via regulation of its metabolism.2,3) As a factor regulating NOS activity in vivo, asymmetric dimethylarginine (ADMA), an endogeneous competitive inhibitor of NOS activFrom the