title: Telmisartan improves vascular function independently of metabolic and antihypertensive effects in hypertensive subjects with impaired glucose tolerance.
abstract: BACKGROUND
  Hypertensive patients with IGT have increased risk for cardiovascular disease and progression to diabetes mellitus. Clinical trials suggest that the ARB telmisartan uniquely possesses PPARγ agonistic properties and improves insulin resistance as well as vascular endothelial dysfunction. The aim of the present study was to compare vascular effects of telmisartan and losartan in relation to their metabolic and antihypertensive effects in hypertensive patients with IGT.
  
  
  METHODS
  24 patients were randomised in a double-blind, prospective, cross-over trial. At baseline and after 12 weeks of either treatment an oGTT, and endothelial function testing was performed.
  
  
  RESULTS
  Endothelial function improved significantly by telmisartan treatment but not by losartan treatment (FMD; T: 7.9 ± 0.7%, vs B: 6.4 ± 0.8, p<0.01; vs L: 6.4 ± 0.6, p<0.001) at almost identical antihypertensive effect of both agents. Insulin resistance assessed by HOMA (T: 2.20 ± 0.47 vs B: 3.04 ± 0.60, p<0.01; vs L: 3.38 ± 0.84, T vs L p<0.05) and ISI120 (T: 0.114 ± 0.003 vs B: 0.092 ± 0.002, p<0.001; vs L: 0.090 ± 0.006, T vs L p<0.01) improved significantly after telmisartan only, as did glucose tolerance (p<0.01). The improvement of the endothelial function observed, significantly depended on pretreatment insulin resistance but was independent of improvements of insulin resistance, blood pressure or glucose tolerance.
  
  
  CONCLUSIONS
  In hypertensive patients with IGT telmisartan compared to losartan improved endothelial function and insulin resistance independently, supporting the hypothesis that glucometabolic and vascular insulin resistance are differentially regulated.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, Medical University of Graz, Austria.
authors.forename: Sabine
authors.initials: S
authors.lastname: Perl
authors.forename: Isabella
authors.initials: I
authors.lastname: Schmölzer
authors.forename: Harald
authors.initials: H
authors.lastname: Sourij
authors.forename: Helga
authors.initials: H
authors.lastname: Pressl
authors.forename: Michaela
authors.initials: M
authors.lastname: Eder
authors.forename: Robert
authors.initials: R
authors.lastname: Zweiker
authors.forename: Thomas C
authors.initials: TC
authors.lastname: Wascher
mesh_terms: D000328:Adult; D000368:Aged; D000959:Antihypertensive Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001562:Benzimidazoles / Q000627:therapeutic use*; D001565:Benzoates / Q000627:therapeutic use*; D018592:Cross-Over Studies; D004311:Double-Blind Method; D005260:Female; D018149:Glucose Intolerance / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D000077333:Telmisartan; D014652:Vascular Diseases / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology*
chemical_list: D000959:Antihypertensive Agents; D001562:Benzimidazoles; D001565:Benzoates; D007004:Hypoglycemic Agents; D000077333:Telmisartan