Impairment of endothelium-dependent relaxation of the isolated basilar artery from streptozotocin-induced diabetic rats.

In the isolated rat basilar artery, acetylcholine (ACh) caused concentration-dependent relaxation. The relaxation induced by ACh was significantly inhibited by NG-nitro-L-arginine (L-NNA) (10(-4) M) or isotonic high K+ medium (30 mM) but not by treatment with indomethacin (3 x 10(-5) M) or glibenclamide (10(-6) M). The relaxation was abolished by the combined treatment with L-NNA and isotonic high K+ (30 mM). The relaxation caused by ACh was significantly attenuated in the basilar artery from streptozotocin (STZ)-induced diabetic rats. L-NNA caused contractile response in the isolated basilar artery and this response was significantly attenuated in diabetic rats. IBMX (3-isobutyl-1-methylxanthine)-induced relaxation response was slightly but significantly attenuated in diabetic rats. The relaxation of the basilar artery caused by sodium nitroprusside was not significantly different between control and diabetic rats. In the present study, we were the first to report that the endothelium-dependent relaxation of the isolated rat basilar artery in response to ACh was significantly impaired during STZ-induced diabetic rats.