title: Alpha-adrenoceptor blockade prevents exercise-induced vasoconstriction of stenotic coronary arteries.
abstract: OBJECTIVE
  The study aimed to evaluate the role of alpha-adrenergic mechanisms during dynamic exercise in both normal and stenotic coronary arteries.
  
  
  BACKGROUND
  Paradoxical vasoconstriction of stenotic coronary arteries has been reported during dynamic exercise and may be due to several factors such as alpha-adrenergic drive, a decreased release of nitric oxide, platelet aggregation with release of serotonin, or a passive collapse of the vessel wall.
  
  
  METHODS
  Twenty-six patients were studied at rest, during two levels of supine bicycle exercise and after 1.6 mg sublingual nitroglycerin. The alpha-blocker phentolamine was given to 16 patients before exercise, five of whom had also taken a beta-adrenergic-blocker the same morning. Ten patients served as controls. The cross-sectional areas of a normal and a stenotic coronary vessel were determined by biplane quantitative coronary arteriography.
  
  
  RESULTS
  In the normal vessel segments, coronary cross-sectional area did not change after phentolamine injection, but increased in all patient groups similarly during exercise. Although coronary vasoconstriction existed in stenotic vessel segments in control patients, phentolamine-treated patients showed exercise-induced vasodilation without difference in patients with and without chronic beta-blockade.
  
  
  CONCLUSIONS
  Exercise-induced vasoconstriction of stenotic coronary arteries is prevented by intracoronary administration of phentolamine. There was no difference in coronary vasomotion between patients receiving phentolamine alone and patients receiving phentolamine in addition to a beta-blocker. This finding suggests that exercise-induced vasoconstriction is mediated not only by endothelial dysfunction but also by alpha-adrenergic mechanisms.
authors.affiliation: Department of Internal Medicine, University Hospital, Zurich, Switzerland.
authors.forename: B K
authors.initials: BK
authors.lastname: Julius
authors.forename: G
authors.initials: G
authors.lastname: Vassalli
authors.forename: L
authors.initials: L
authors.lastname: Mandinov
authors.forename: O M
authors.initials: OM
authors.lastname: Hess
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000008:administration & dosage* / Q000009:adverse effects; D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage / Q000009:adverse effects; D000328:Adult; D000368:Aged; D001262:Atenolol / Q000008:administration & dosage / Q000009:adverse effects; D006328:Cardiac Catheterization; D017023:Coronary Angiography / Q000187:drug effects; D003326:Coronary Circulation / Q000187:drug effects* / Q000502:physiology; D003327:Coronary Disease / Q000188:drug therapy* / Q000503:physiopathology; D005080:Exercise Test / Q000187:drug effects*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D008297:Male; D008790:Metoprolol / Q000008:administration & dosage / Q000009:adverse effects; D008875:Middle Aged; D005996:Nitroglycerin / Q000008:administration & dosage / Q000009:adverse effects; D010646:Phentolamine / Q000008:administration & dosage* / Q000009:adverse effects; D011292:Premedication; D014661:Vasoconstriction / Q000187:drug effects* / Q000502:physiology; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000009:adverse effects
chemical_list: D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D014665:Vasodilator Agents; D001262:Atenolol; D005996:Nitroglycerin; D008790:Metoprolol; D010646:Phentolamine