title: Characteristics of coronary endothelial dysfunction in experimental diabetes.
abstract: OBJECTIVE
  To study the influence of diabetes on the endothelium-dependent vasodilation in the coronary arterial bed.
  
  
  METHODS
  The effects of acetylcholine (ACh 2-36 pmol.kg-1; 18 nmol.1(-1)-9.8 mumol.1(-1); 0.1-10 mumol.1(-1), L-arginine (1 mmol.1(-1) and sodium nitroprusside (1 nmol.1(-1)-100 mumol.1(-1)) were measured on coronary conductivity, vascular tone and cGMP release (RIA) in healthy and diabetic dogs.
  
  
  RESULTS
  ACh-mediated (in cumulative intra-arterial infusion) increase in coronary conductivity was reduced (P < 0.01) in the diabetic dogs in vivo, whereas no increase in cGMP release was observed in isolated diabetic coronaries (P < 0.05) which could not be enhanced by L-arginine (P < 0.05). Inhibition of cyclo-oxygenase after 20 min further impaired (P < 0.01) responsiveness to ACh in vivo and diminished the ACh response in isolated coronary strips of the diabetic dogs, but not in those of the controls. Relaxation in response to sodium nitroprusside was not altered by diabetes.
  
  
  CONCLUSIONS
  Diminished vasodilation in diabetes is due to a defect in endothelial nitric oxide production and action. Vasodilating prostanoids do not sufficiently compensate this defect.
authors.affiliation: National Institute of Cardiology, Budapest, Hungary.
authors.forename: M Z
authors.initials: MZ
authors.lastname: Koltai
authors.forename: P
authors.initials: P
authors.lastname: Hadházy
authors.forename: I
authors.initials: I
authors.lastname: Pósa
authors.forename: E
authors.initials: E
authors.lastname: Kocsis
authors.forename: G
authors.initials: G
authors.lastname: Winkler
authors.forename: P
authors.initials: P
authors.lastname: Rösen
authors.forename: G
authors.initials: G
authors.lastname: Pogátsa
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001120:Arginine / Q000494:pharmacology*; D003326:Coronary Circulation / Q000187:drug effects; D003331:Coronary Vessels / Q000187:drug effects / Q000378:metabolism*; D006152:Cyclic GMP / Q000378:metabolism; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000503:physiopathology; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D005260:Female; D007052:Ibuprofen / Q000494:pharmacology; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D009569:Nitric Oxide / Q000096:biosynthesis / Q000502:physiology*; D009599:Nitroprusside / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D016861:Cyclooxygenase Inhibitors; D014665:Vasodilator Agents; D009599:Nitroprusside; D009569:Nitric Oxide; D001120:Arginine; D006152:Cyclic GMP; D000109:Acetylcholine; D007052:Ibuprofen; D007213:Indomethacin