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Decrease in endothelium-dependent relaxation and levels of cyclic nucleotides in aorta from rabbits with
T Abiru1, Y Watanabe, K Kamata
1Research and Development Division, Yamasa Shoyu Co., Ltd., Chiba, Japan.
Research Communications in Chemical Pathology and Pharmacology
|April 1, 1990
Summary
Diabetes mellitus impairs vascular relaxation by reducing cyclic GMP production in rabbit aorta. This suggests endothelial dysfunction, not altered guanylate cyclase activity, is responsible for reduced relaxation in diabetic blood vessels.
Area of Science:
- Vascular biology
- Endocrinology
- Pharmacology
Background:
- Diabetes mellitus is associated with cardiovascular complications.
- Endothelial dysfunction contributes to impaired vascular relaxation in diabetes.
Purpose of the Study:
- To investigate the impact of diabetes mellitus on vascular relaxation response.
- To compare acetylcholine (ACh)-induced relaxation and cyclic nucleotide production in diabetic and control rabbit aortas.
Main Methods:
- Comparison of ACh-induced relaxation in aortic rings with endothelium from diabetic and control rabbits.
- Assessment of cyclic guanosine monophosphate (cGMP) and cyclic adenosine monophosphate (cAMP) levels.
- Evaluation of sodium nitroprusside (SNP)-induced relaxation in aortic rings without endothelium.
Main Results:
- ACh-induced relaxation was significantly reduced in diabetic rabbit aortas.
- Hemoglobin pretreatment shifted the ACh concentration-response curve in control aortas, mimicking diabetic responses.
- Basal and ACh-induced cGMP production were markedly lower in diabetic aortas, while cAMP levels remained unchanged.
- SNP-induced relaxation was similar in both groups, indicating preserved smooth muscle function.
Conclusions:
- Diabetes mellitus impairs endothelium-dependent vascular relaxation.
- The primary defect appears to be in the endothelium, specifically reduced release of endothelium-derived relaxing factor (EDRF).
- This impairment leads to decreased cGMP production and contributes to the observed relaxation deficit in diabetic aortas.