title: Effective blood pressure treatment improves LDL-cholesterol susceptibility to oxidation in patients with essential hypertension.
abstract: OBJECTIVE
  LDL-cholesterol particles from hypertensive patients exhibit enhanced susceptibility to in vitro oxidation, an abnormality thought to increase cardiovascular risk. We tested whether blood pressure (BP) normalization can reverse this abnormality.
  
  
  METHODS
  Double-blind, randomized pharmacological intervention trial.
  
  
  METHODS
  Clinical research centre. Subjects. A total of 29 nondiabetic, normolipidaemic patients with essential hypertension (BP= 151 +/- 3/99 +/- 1 mmHg) and 11 normotensive controls (BP=125 +/- 3/85 +/- 1 mmHg) matched for gender, age, obesity, glucose tolerance and lipid profile. Intervention. Anti-hypertensive treatment for 3 months with a calcium-antagonist in randomized combination with either an ACE inhibitor or a beta-blocker.
  
  
  METHODS
  Lag phase of copper-induced LDL oxidation, cell-mediated (human umbilical vein endothelium) generation of malondialdehyde (MDA) by LDL and vitamin E content in LDL.
  
  
  RESULTS
  At baseline in hypertensives versus controls, lag phase was shorter (89 +/- 3 vs. 107 +/- 6 min, P < 0.04), MDA generation was higher (5.8 +/- 0.1 vs. 5.1 +/- 0.2 nmol L(-1), P=0.002), and vitamin E was reduced (6.40 +/- 0.05 vs. 6.67 +/- 0.11 microg mg(-1), P=0.03). At 3 months, BP was normalized (124 +/- 3/81 +/- 1, P < 0.0001 vs. baseline, P=ns versus controls), lag phase was prolonged (to 98 +/- 3 min, P=0.0005), MDA generation was reduced (5.6 +/- 0.1 nmol L-1, P = 0.001), and vitamin E was increased (6.53 +/- 0.05 microg mg(-1), P=0.003), with no significant differences between the randomized groups.
  
  
  CONCLUSIONS
  In nondiabetic, nonobese, normolipidaemic patients with essential hypertension, LDL susceptibility to copper- and cell-mediated oxidation is increased. BP normalization is associated with a significant improvement, but not a full reversal, of this abnormality.
authors.affiliation: CNR Institute of Clinical Physiology and Department of Internal Medicine, University of Pisa, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Quiñones-Galvan
authors.forename: A
authors.initials: A
authors.lastname: Pucciarelli
authors.forename: A
authors.initials: A
authors.lastname: Fratta-Pasini
authors.forename: U
authors.initials: U
authors.lastname: Garbin
authors.forename: F
authors.initials: F
authors.lastname: Franzoni
authors.forename: F
authors.initials: F
authors.lastname: Galetta
authors.forename: A
authors.initials: A
authors.lastname: Natali
authors.forename: L
authors.initials: L
authors.lastname: Cominacini
authors.forename: E
authors.initials: E
authors.lastname: Ferrannini
mesh_terms: D000328:Adult; D000959:Antihypertensive Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001262:Atenolol / Q000009:adverse effects / Q000627:therapeutic use; D008078:Cholesterol, LDL / Q000097:blood*; D004311:Double-Blind Method; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000188:drug therapy*; D007211:Indoles / Q000009:adverse effects / Q000627:therapeutic use; D008297:Male; D008315:Malondialdehyde / Q000097:blood*; D008875:Middle Aged; D009543:Nifedipine / Q000009:adverse effects / Q000627:therapeutic use; D018384:Oxidative Stress / Q000187:drug effects; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014700:Verapamil / Q000009:adverse effects / Q000627:therapeutic use
chemical_list: D000959:Antihypertensive Agents; D008078:Cholesterol, LDL; D007211:Indoles; D017392:Thiobarbituric Acid Reactive Substances; C052035:trandolapril; D008315:Malondialdehyde; D001262:Atenolol; D014700:Verapamil; D009543:Nifedipine