title: AT1-receptor blockade improves augmentation index: a double-blind, randomized, controlled study.
abstract: OBJECTIVE
  Arterial hypertension leads to vascular structural and functional adaptive processes that are influenced by angiotensin II. To analyze the effects of AT receptor blockade on vascular function we determined augmentation index.
  
  
  METHODS
  A total of 60 patients (53 +/- 10 years) with essential hypertension mean [blood pressure (BP) 173 +/- 9/102 +/- 3 mmHg] were randomized to 6 weeks double-blind therapy with either valsartan 80 mg, hydrochlorothiazide (HCTZ) 25 mg or placebo once daily. Radial artery pressure wave was determined by applanation tonometry before and after therapy. The central aortic pressure wave and augmentation index were derived by a generalized transfer function.
  
  
  RESULTS
  Active therapy similarly reduced systolic and diastolic blood pressure (SBP, DBP) (valsartan: -22 +/- 18/-11 +/- 11 mmHg, HCTZ: -22 +/- 23/-14 +/- 14 mmHg, all P < 0.001). However, only valsartan, but no HCTZ reduced the augmentation index (valsartan: from 148 +/- 18 to 126 +/- 24, < 0.001; HCTZ: from 145 +/- 19 to 142 +/- 18, NS). Augmentation index reduction was greater with valsartan (-22 +/- 11) than with HCTZ (-3 +/- 11) and placebo (0 +/- 13) (P < 0.01 for pairwise comparison of valsartan versus HCTZ and placebo after Bonferroni correction). Differences remained significant after taking changes in supine BP into account (covariance, P < 0.01).
  
  
  CONCLUSIONS
  Blood pressure reduction with the AT receptor antagonist valsartan but not with hydrochlorothiazide reduced the augmentation index in essential hypertension.
authors.affiliation: Department of Medicine IV, University of Erlangen-Nürnberg, Germany.
authors.forename: Arnfried U
authors.initials: AU
authors.lastname: Klingbeil
authors.forename: Stefan
authors.initials: S
authors.lastname: John
authors.forename: Markus P
authors.initials: MP
authors.lastname: Schneider
authors.forename: Johannes
authors.initials: J
authors.lastname: Jacobi
authors.forename: Gottfried
authors.initials: G
authors.lastname: Weidinger
authors.forename: Roland E
authors.initials: RE
authors.lastname: Schmieder
mesh_terms: D000328:Adult; D000368:Aged; D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001011:Aorta / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects; D003971:Diastole; D004232:Diuretics; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D006852:Hydrochlorothiazide / Q000627:therapeutic use*; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D011674:Pulse; D017534:Radial Artery / Q000503:physiopathology; D044140:Receptor, Angiotensin, Type 1; D049993:Sodium Chloride Symporter Inhibitors / Q000627:therapeutic use*; D013599:Systole; D013777:Tetrazoles / Q000627:therapeutic use*; D014633:Valine / Q000031:analogs & derivatives* / Q000627:therapeutic use*; D000068756:Valsartan
chemical_list: D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents; D004232:Diuretics; D044140:Receptor, Angiotensin, Type 1; D049993:Sodium Chloride Symporter Inhibitors; D013777:Tetrazoles; D006852:Hydrochlorothiazide; D000068756:Valsartan; D014633:Valine