RESPONSES OF CEREBRAL ARTERIOLES TO ACTIVATION OF BETA-ADRENERGIC RECEPTORS DURING DIABETES-MELLITUS

Background and Purpose Diabetes mellitus impairs reactivity of large p eripheral arteries and arterioles to activation of beta-adrenergic rec eptors. The goal of this study was to determine whether diabetes melli tus alters dilatation of cerebral arterioles to activation of beta-adr energic receptors. Methods In vivo diameter of pial arterioles was mea sured in nondiabetic and diabetic (streptozotocin 50 to 60 mg/kg IP) r ats during superfusion with isoproterenol, forskolin, and nitroglyceri n. In addition, we examined the contribution of nitric oxide or a nitr ic oxide-containing compound in dilatation of pial arterioles in respo nse to the agonists. Results Dilatation of pial arterioles in response to isoproterenol was significantly less in diabetic compared with non diabetic rats (3 +/- 2% versus 14 +/- 1%, respectively, for 1.0 mumol/ L isoproterenol). In contrast, dilatation of pial arterioles in respon se to nitroglycerin and forskolin was similar in nondiabetic and diabe tic rats. Furthermore, dilatation of pial arterioles in nondiabetic ra ts in response to isoproterenol and forskolin was not related to the s ynthesis and release of nitric oxide or a nitric oxide-containing comp ound. Conclusions The findings of the present studies suggest that dia betes mellitus impairs dilatation of cerebral resistance arterioles in response to activation of beta-adrenergic receptors. Impairment of be ta-adrenergic-mediated dilatation of cerebral arterioles during diabet es mellitus does not appear to be related to an alteration in cyclic a denosine monophosphate, since forskolin produced similar vasodilatatio n in nondiabetic and diabetic rats.