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Characteristics of coronary endothelial dysfunction in experimental diabetes
M Z Koltai1, P Hadházy, I Pósa
1National Institute of Cardiology, Budapest, Hungary.
Cardiovascular Research
|April 1, 1997
Summary
Diabetes impairs endothelium-dependent vasodilation in coronary arteries due to reduced nitric oxide production. This defect in vasodilation is not compensated by vasodilating prostanoids.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Pharmacology
Background:
- Diabetes mellitus is associated with endothelial dysfunction.
- Endothelial dysfunction contributes to cardiovascular complications in diabetes.
Purpose of the Study:
- To investigate the impact of diabetes on endothelium-dependent vasodilation in the coronary arterial bed.
- To elucidate the mechanisms underlying impaired vasodilation in diabetic canine coronary arteries.
Main Methods:
- Assessed coronary conductivity, vascular tone, and cyclic guanosine monophosphate (cGMP) release in healthy and diabetic dogs.
- Administered acetylcholine (ACh), L-arginine, and sodium nitroprusside.
- Utilized radioimmunoassay (RIA) for cGMP measurement and cyclooxygenase inhibition.
Main Results:
- Acetylcholine-mediated coronary vasodilation was significantly reduced in diabetic dogs.
- Isolated diabetic coronary arteries showed no increase in cGMP release in response to ACh, unresponsive to L-arginine.
- Cyclooxygenase inhibition further impaired ACh responsiveness in diabetic dogs in vivo and in vitro.
- Sodium nitroprusside-induced relaxation was unaffected by diabetes.
Conclusions:
- Diabetes causes a defect in endothelial nitric oxide production and action, leading to diminished coronary vasodilation.
- Vasodilating prostanoids do not adequately compensate for the impaired nitric oxide pathway in diabetes.