EFFECT OF DIABETES-MELLITUS ON RESPONSES OF THE RAT BASILAR ARTERY TO ACTIVATION OF BETA-ADRENERGIC RECEPTORS

The goal of this study was to determine whether diabetes mellitus alters reactivity of the basilar artery in vivo to activation of beta-adrenergic receptors. We measured diameter of the basilar artery in non-diabetic and diabetic (streptozotocin 50-60 mg/kg i.p.) rats during superfusion with isoproterenol and norepinephrine, which dilate cerebral blood vessels via activation of beta-adrenergic receptors. Dilatation of the basilar artery in response to isoproterenol and norepinephrine was significantly less in diabetic compared to non-diabetic rats. To determine whether impaired dilatation of the basilar artery in diabetic rats in response to isoproterenol and norepinephrine was related to an alteration in catalytic activity of adenylate cyclase, we examined dilatation of the basilar artery in response to forskolin, a direct activator of adenylate cyclase. In contrast to that observed for isoproterenol and norepinephrine, forskolin produced similar dilatation of the basilar artery in non-diabetic and diabetic rats. Thus, the findings of the present study suggest that diabetes mellitus impairs dilatation of the basilar artery in vivo in response to activation of beta-adrenergic receptors. In addition, impairment of beta-adrenergic mediated dilatation of the basilar artery during diabetes mellitus does not appear to be related to an alteration in catalytic activity of adenylate cyclase.