title: Telmisartan decreases plasma levels of asymmetrical dimethyl-L-arginine and improves lipid and glucose metabolism and vascular function.
abstract: Telmisartan is an angiotensin II receptor blocker (ARB) and also an activator of peroxisome proliferator-activated receptor-gamma (PPAR-gamma). We investigated whether telmisartan improves vascular endothelial function in patients with essential hypertension with the production of endothelial nitric oxide synthase (eNOS) through PPAR-gamma.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-gamma, suggesting that this agent improves vascular endothelial function via its pleiotropic effects, a mechanism that is different from its hypotensive effects.
authors.affiliation: Department of Cardiology, Tokushima University, Tokushima, Japan.
authors.forename: Yoshifumi
authors.initials: Y
authors.lastname: Ono
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Nakaya
authors.forename: Shigenobu
authors.initials: S
authors.lastname: Bando
authors.forename: Takeshi
authors.initials: T
authors.lastname: Soeki
authors.forename: Susumu
authors.initials: S
authors.lastname: Ito
authors.forename: Masataka
authors.initials: M
authors.lastname: Sata
mesh_terms: D000284:Administration, Oral; D000368:Aged; D047228:Angiotensin II Type 1 Receptor Blockers / Q000008:administration & dosage / Q000627:therapeutic use*; D001120:Arginine / Q000031:analogs & derivatives* / Q000037:antagonists & inhibitors / Q000097:blood; D001562:Benzimidazoles / Q000008:administration & dosage / Q000627:therapeutic use*; D001565:Benzoates / Q000008:administration & dosage / Q000627:therapeutic use*; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism*; D001794:Blood Pressure / Q000187:drug effects; D008078:Cholesterol, LDL / Q000097:blood* / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D052250:Nitric Oxide Synthase Type III / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D047495:PPAR gamma / Q000187:drug effects / Q000378:metabolism; D000077333:Telmisartan; D016896:Treatment Outcome
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D001562:Benzimidazoles; D001565:Benzoates; D001786:Blood Glucose; D008078:Cholesterol, LDL; D047495:PPAR gamma; C018524:N,N-dimethylarginine; D001120:Arginine; D052250:Nitric Oxide Synthase Type III; D000077333:Telmisartan