L-ARGININE DOES NOT RESTORE DILATATION OF THE BASILAR ARTERY DURING DIABETES-MELLITUS

The goal of this study was to test the hypothesis that administration of L-arginine, a substrate for the synthesis of nitric oxide, restores endothelium-dependent dilatation of the basilar artery during diabete s mellitus. We measured the diameter of the basilar artery in vivo in nondiabetic and diabetic (streptozotocin; 50-60 mg/kg i.p.) rats in re sponse to endothelium-dependent agonists (acetylcholine and bradykinin ) and an endothelium-independent agonist (nitroglycerin) before and du ring application of L-arginine. Topical application of acetylcholine ( 1.0 and 10 mu M) and bradykinin (1.0 and 10 mu M) produced dilatation in nondiabetic rats of the basilar artery which was impaired in diabet ic rats. Topical application of nitroglycerin (0.1 and 1.0 mu M) produ ced similar dilatation of the basilar artery in nondiabetic and diabet ic rats. Topical application of L-arginine (0.1 and 3 mM) did not enha nce dilatation of the basilar artery in response to acetylcholine and bradykinin in diabetic rats. Thus, impairment of dilatation of the bas ilar artery in diabetic rats in response to acetylcholine and bradykin in appears to be related to a mechanism unrelated to the availability of L-arginine for nitric oxide synthase.