title: Vitamin C improves endothelial dysfunction of epicardial coronary arteries in hypertensive patients.
abstract: BACKGROUND
  There is evidence for increased formation of free radicals in patients with hypertension, raising the possibility that NO is inactivated by free radicals, which impairs coronary endothelial function. Therefore, we tested the hypothesis that the antioxidant vitamin C could improve abnormal endothelial function of coronary arteries in patients with hypertension.
  
  
  RESULTS
  In 22 hypertensive patients without relevant coronary artery stenoses, endothelium-dependent vascular responses of the left anterior descending coronary artery (LAD) to acetylcholine (0.01, 0.1, and 1.0 micromol/L) were determined before and immediately after intravenous infusion of 3 g vitamin C (17 patients) or placebo (5 patients). In a subgroup of 10 patients, papaverine-induced flow-dependent vasodilation (FDD) was measured before and after vitamin C (5 patients) or placebo (5 patients) infusion. Segmental responses of the coronary artery luminal area were analyzed with quantitative coronary angiography. Before vitamin C infusion, the mean changes of LAD luminal areas at increasing doses of acetylcholine were -6.1+/-2.2%, -15.2+/-4.9%, and -33.9+/-8.1% (negative numbers symbolize vasoconstriction) and during FDD, 5.4+/-1.0%. The vasoconstrictor response during acetylcholine was reduced and FDD was augmented by vitamin C. After vitamin C infusion, LAD luminal areas changed by -3.2+/-2.3%, -5.8+/-3.6%, and -10.2+/-5.6% (P<.05, acetylcholine) and 17.8+/-2.8% (P<.05, FDD). Doppler flow velocity (during baseline, acetylcholine, and FDD) was not significantly affected by vitamin C.
  
  
  CONCLUSIONS
  Vitamin C improves the endothelium-dependent vasomotor capacity of coronary arteries in patients with hypertension and patent coronary arteries. These findings suggest that increased oxidative stress contributes to endothelial dysfunction in hypertensive patients.
authors.affiliation: Medical Clinic, Department of Cardiology, University of Freiburg, Germany.
authors.forename: U
authors.initials: U
authors.lastname: Solzbach
authors.forename: B
authors.initials: B
authors.lastname: Hornig
authors.forename: M
authors.initials: M
authors.lastname: Jeserich
authors.forename: H
authors.initials: H
authors.lastname: Just
mesh_terms: D000109:Acetylcholine / Q000627:therapeutic use; D000328:Adult; D000368:Aged; D000975:Antioxidants / Q000627:therapeutic use*; D001158:Arteries / Q000187:drug effects / Q000503:physiopathology; D001205:Ascorbic Acid / Q000627:therapeutic use*; D003331:Coronary Vessels / Q000187:drug effects* / Q000503:physiopathology; D004359:Drug Therapy, Combination; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D010208:Papaverine / Q000627:therapeutic use; D010496:Pericardium; D014665:Vasodilator Agents / Q000627:therapeutic use
chemical_list: D000975:Antioxidants; D014665:Vasodilator Agents; D010208:Papaverine; D000109:Acetylcholine; D001205:Ascorbic Acid