Impairment of endothelium-dependent dilatation of the basilar artery during diabetes mellitus

The goal of this study was to determine whether responses of the basilar artery are altered during diabetes mellitus. We measured the diameter of the basilar artery in vivo in non-diabetic and diabetic rats (streptozotocin; 50-60 mg/kg i.p.). Responses of the basilar artery to agonists, which presumably produce dilatation by releasing endothelium-derived relaxing factor (EDRF), were impaired in diabetic rats compared to non-diabetic rats. Acetylcholine (1.0 and 10 μM) dilated the basilar artery by 13 ± 2 and 26 ± 4% (means ± S.E.M.), respectively, in non-diabetic rats, but by only 13 ± 1 and 9 ± 2%, respectively, in diabetic rats (P < 0.05). Bradykinin (1.0 and 10 μM) dilated the basilar artery by 14 ± 2 and 35 ± 6 % (means ± S.E.M.), respectively, in non-diabetic rats, but by only 5 ± 1 and 6± 2%, respectively, in diabetic rats (P < 0.05). The response to nitroglycerin was similar in non-diabetic and diabetic rats. Thus, impairment of vasodilatation in diabetic rats in response to acetylcholine and bradykinin is not related to non-specific impaired of vasodilation than impaired dilator responses of the basilar artery in response to acetylcholine and bradykinin in diabetic rats may be related to the activation of the thromboxane A₂-prostaglandin H₂ receptor. SQ 29548 (a specific thromboxane A₂-prostaglandin H₂ receptor antagonist) did not alter responses of the basilar artery to acetylcholine and bradykinin. These findings suggest that diabetes mellitus impairs endothelium-dependent dilation of the basilar artery. In addition, the mechanism of impaired responses of the basilar artery during diabetes mellitus does not appear to be related to the activation of the thromboxane A₂-prostaglandin H₂ receptor.