Endothelium-dependent relaxation produced by acetylcholine or A23187 was significantly attenuated in diabetic rat aortae compared to controls, while endothelium-independent relaxation was preserved.
Does diabetes impair endothelium-dependent relaxation in rat aortae?
Diabetes leads to a specific impairment of endothelium-dependent relaxation in rat aortae, highlighting a mechanism for vascular reactivity alterations in diabetes.
Diabetes mellitus is known to produce alterations in vascular reactivity. The present study examined the effects of endothelium-dependent and endothelium-independent relaxing substances on thoracic aorta from control and spontaneously diabetic rats. 2. Endothelium-dependent relaxation produced by acetylcholine or the calcium ionophore, A23187, in aortic rings precontracted with phenylephrine was significantly attenuated in diabetic vessels. 3. Relaxations produced by sodium nitroprusside or adenosine in diabetic preparations were comparable to those in control vessels. 4. The results show that diabetes leads to a specific impairment of endothelial-dependent relaxation.
Durante et al. (Wed,) conducted a other in Diabetes mellitus. Acetylcholine, A23187, sodium nitroprusside, adenosine vs. Control rats was evaluated on Endothelium-dependent and endothelium-independent relaxation in thoracic aorta. Endothelium-dependent relaxation produced by acetylcholine or A23187 was significantly attenuated in diabetic rat aortae compared to controls, while endothelium-independent relaxation was preserved.