ENDOTHELIUM-DERIVED HYPERPOLARIZING FACTOR DOES NOT CONTRIBUTE TO THEDECREASE IN ENDOTHELIUM-DEPENDENT RELAXATION IN THE AORTA OF STREPTOZOTOCIN-INDUCED DIABETIC RATS

1. We examined the contribution of endothelium-derived hyperpolarizing factor (EDHF) to the impairment of endothelium-dependent relaxation c aused by acetylcholine (ACh) in the aorta of streptozotocin-induced di abetic rats, by using N-omega-L-nitro-arginine methylester (L-NAME) an d tetraethylammonium chloride (TEA) to inhibit nitric oxide (NO) and E DHF, respectively. 2. ACh-induced relaxation of the aorta decreased in diabetic rats. In contrast, sodium nitroprusside-induced relaxation w as the same in diabetic rats and control rats. 3. Treatment with 5 x 1 0(-7) M L-NAME resulted in a right shift of the dose-response curves o f ACh-induced relaxation in the aorta. The shift was greater in the co ntrol aorta. 4. Treatment with 5 x 10(-4) M TEA resulted in a similar right shift in both the control and diabetic aorta. 5. Therefore, whil e endothelium-derived NO appears to contribute to the impairment of AC h-induced endothelium-dependent relaxation in the aorta of diabetic ra ts, EDHF does not.