title: Anti-inflammatory and metabolic effects of candesartan in hypertensive patients.
abstract: BACKGROUND
  Angiotensin II type 1 (AT1) receptor blocker therapy prevented or retarded the progression of coronary heart disease. The mechanisms of this benefit may relate to the ability of AT1 receptor blockers to reduce inflammation and insulin resistance.
  
  
  METHODS
  We administered placebo or candesartan 16 mg daily during 2 months to 45 patients with mild to moderate hypertension. This study was randomized, double-blind, placebo-controlled, crossover in design.
  
  
  RESULTS
  Candesartan therapy significantly lowered both systolic and diastolic blood pressure. Compared with placebo, candesartan therapy significantly lowered plasma hsCRP levels relative to baseline measurements from 1.10 to 0.70 mg/l (P=0.024) and soluble CD40 ligand levels by 30+/-11% (P<0.001). There were significant inverse correlations between body mass index and baseline plasma adiponectin levels (r=-0.480, P=0.009). There were significant correlations between baseline adiponectin levels and baseline insulin (r=-0.317, P=0.034) or baseline Quantitative Insulin-Sensitivity Check Index (QUICKI), a surrogate index of insulin sensitivity (r=0.371, P=0.012). Compared with placebo, candesartan therapy significantly lowered fasting insulin levels (P=0.011) and increased plasma levels of adiponectin by 15+/-4% (P=0.012) and increased QUICKI by 8+/-2% (P=0.007). There were significant correlations between percent changes in adiponectin levels and percent changes in insulin (r=-0.340, P=0.022) or QUICKI (r=0.325, P=0.029).
  
  
  CONCLUSIONS
  Candesartan therapy significantly reduced inflammation and increased adiponectin levels and improved insulin sensitivity in hypertensive patients.
authors.affiliation: Cardiology, Gachon Medical School, Incheon, South Korea. kwangk@ghil.com
authors.forename: Kwang Kon
authors.initials: KK
authors.lastname: Koh
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Quon
authors.forename: Seung Hwan
authors.initials: SH
authors.lastname: Han
authors.forename: Wook-Jin
authors.initials: WJ
authors.lastname: Chung
authors.forename: Yonghee
authors.initials: Y
authors.lastname: Lee
authors.forename: Eak Kyun
authors.initials: EK
authors.lastname: Shin
mesh_terms: D052242:Adiponectin / Q000097:blood; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology* / Q000627:therapeutic use*; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use; D001562:Benzimidazoles / Q000494:pharmacology* / Q000627:therapeutic use*; D001713:Biphenyl Compounds; D001794:Blood Pressure / Q000187:drug effects; D002097:C-Reactive Protein / Q000032:analysis / Q000187:drug effects; D003327:Coronary Disease / Q000517:prevention & control; D018592:Cross-Over Studies; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D013777:Tetrazoles / Q000494:pharmacology* / Q000627:therapeutic use*; D016896:Treatment Outcome
chemical_list: D052242:Adiponectin; D047228:Angiotensin II Type 1 Receptor Blockers; D000893:Anti-Inflammatory Agents; D001562:Benzimidazoles; D001713:Biphenyl Compounds; D013777:Tetrazoles; D002097:C-Reactive Protein; C081643:candesartan