title: Amlodipine improves endothelial function and metabolic parameters in patients with hypertension.
abstract: BACKGROUND
  Reciprocal relationships between endothelial dysfunction and insulin resistance imply that improvement in endothelial dysfunction will have beneficial metabolic consequences. We hypothesized that amlodipine therapy in hypertensive subjects will improve endothelial dysfunction and metabolic parameters.
  
  
  METHODS
  Amlodipine (10 mg daily for 8 weeks) or placebo was given to each 45 patients with mild to moderate hypertension in a randomized, double-blind, placebo-controlled, and parallel study. Age, sex, and body mass index were matched.
  
  
  RESULTS
  Amlodipine therapy significantly reduced systolic and diastolic blood pressure and increased HDL-cholesterol to greater extent than placebo therapy (all P<0.001). Amlodipine therapy significantly improved flow-mediated dilator response to hyperemia and reduced plasma malondialdehyde levels to a greater extent than placebo (P<0.001 and P=0.035). Amlodipine therapy significantly increased plasma adiponectin levels (P=0.009) and decreased plasma leptin and resistin levels (P<0.001 and P=0.025, respectively) to a greater extent than placebo. Correlations were noted between percent changes in adiponectin levels and percent changes in HDL-cholesterol (r=0.348, P=0.019) and QUICKI (r=0.326, P=0.029) following amlodipine therapy. Only changes in HDL-cholesterol (beta=0.469, P=0.019) and QUICKI (beta=1.786, P=0.069) were independent predictors of changes in adiponectin levels (multivariate regression analysis). We also observed inverse correlations between percent changes in leptin levels and percent changes in QUICKI (r=-0.569, P<0.001) following amlodipine therapy with changes in QUICKI (beta=1.810, P<0.001) as an independent predictor of changes in leptin levels.
  
  
  CONCLUSIONS
  Amlodipine therapy improves blood pressure, endothelial function, and metabolic parameters in patients with hypertension.
authors.affiliation: Gil Medical Center, Gachon University, Incheon, Korea. kwangk@gilhospital.com
authors.forename: Kwang Kon
authors.initials: KK
authors.lastname: Koh
authors.forename: Seung Hwan
authors.initials: SH
authors.lastname: Han
authors.forename: Jeong Yeal
authors.initials: JY
authors.lastname: Ahn
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; D017311:Amlodipine / Q000627:therapeutic use*; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood*; D008076:Cholesterol, HDL / Q000097:blood / Q000187:drug effects; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000187:drug effects*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000378:metabolism; D020738:Leptin / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D010919:Placebos; D012044:Regression Analysis; D052243:Resistin / Q000097:blood; D018709:Statistics, Nonparametric; D016896:Treatment Outcome
chemical_list: D052242:Adiponectin; D000959:Antihypertensive Agents; D015415:Biomarkers; D008076:Cholesterol, HDL; D020738:Leptin; D010919:Placebos; D052243:Resistin; D017311:Amlodipine; D008315:Malondialdehyde