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Cardiovascular Research 1997 34(1):157-163; doi:10.1016/S0008-6363(97)00050-3
© 1997 by European Society of Cardiology
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Copyright © 1997, European Society of Cardiology

Characteristics of coronary endothelial dysfunction in experimental diabetes

Mária Zsófia Koltaia,*, Pál Hadházyb, Ildikó Pósaa, Erzsébet Kocsisa, Gábor Winklerc, Peter Rösend and Gábor Pogátsaa

aNational Institute of Cardiology, PO Box 9-88, H-1450 Budapest, Hungary
bDepartment of Pharmacodynamics, Semmelweiss Medical School, Budapest, Hungary
cSt. John Municipal Hospital, Budapest, Hungary
dDiabetes Research Institute, Düsseldorf, Germany

* Corresponding author. Tel.: +36 (1) 18-5681; fax: +36 (1) 215-7277.

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·l–1–9.8 µmol·l–1; 0.1–10 µmol·l–1), L-arginine (1 mmol·l–1) and sodium nitroprusside (1 nmol·l–1–100 µmol·l–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.

KEYWORDS Diabetes; Coronary artery; Nitric oxide; Prostaglandins; Dog


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