title: Treatment of hypertension in metabolic syndrome subjects with amlodipine and olmesartan-effects on oxidized non-esterified free fatty acids and cytokine production.
abstract: OBJECTIVE
  Angiotensin II increases activation of oxidative signaling and vascular inflammatory gene expression, and interruption of the renin-angiotensin system has been considered more vasculoprotective than use of calcium channel antagonists and other anti-hypertensive therapies. Despite these putative mechanisms, amlodipine is equally efficacious as other therapies in reducing cardiovascular events.
  
  
  METHODS
  Double-blind, controlled trial, designed to investigate the effects of 2-months treatment with amlodipine and olmesartan on oxidized non-esterified fatty acids (ox-NEFA), and lipopolysaccharide-stimulated cytokine production in whole blood among 23 hypertensive subjects with the metabolic syndrome.
  
  
  RESULTS
  Treatment with olmesartan was no different than amlodipine in changing concentrations of total oxidized fatty acids (p = 0.37), total ox-NEFA (p = 0.43) and 9, 10, 11, 12, 13, 14, 15 and 16 ox-NEFA concentrations. In contrast, 8 ox-NEFA increased (median [interquartile ranges] by 45.2% [5.3 to 50.0] in olmesartan-treated subjects) compared with a decrease of 18.4% (-45.1-13.9) in amlodipine-treated subjects (p = 0.03). Lipopolysaccharide-stimulated cytokine production and levels of soluble cellular adhesion molecules did not change with either treatment.
  
  
  CONCLUSIONS
  Despite experimental data that demonstrates that angiotensin receptor antagonists reduce cellular oxidant stress and inflammation, olmesartan was not different than amlodipine in changing ox-NEFA and inflammatory markers in hypertensive subjects with the metabolic syndrome.
authors.affiliation: Department of Medicine, SUNY Downstate, Brooklyn, NY 11203, USA. robert.rosenson@downstate.edu
authors.forename: Robert S
authors.initials: RS
authors.lastname: Rosenson
mesh_terms: D000328:Adult; D000368:Aged; D017311:Amlodipine / Q000494:pharmacology*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D000959:Antihypertensive Agents / Q000494:pharmacology*; D015815:Cell Adhesion Molecules / Q000378:metabolism; D016207:Cytokines / Q000096:biosynthesis; D004311:Double-Blind Method; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy*; D007093:Imidazoles / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D024821:Metabolic Syndrome / Q000150:complications / Q000188:drug therapy; D008875:Middle Aged; D000068557:Olmesartan Medoxomil; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects; D013777:Tetrazoles / Q000494:pharmacology*
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000959:Antihypertensive Agents; D015815:Cell Adhesion Molecules; D016207:Cytokines; D005230:Fatty Acids, Nonesterified; D007093:Imidazoles; D008070:Lipopolysaccharides; D013777:Tetrazoles; D017311:Amlodipine; D000068557:Olmesartan Medoxomil