Wg. Mayhan, EFFECT OF DIABETES-MELLITUS ON RESPONSES OF THE RAT BASILAR ARTERY TOACTIVATION OF BETA-ADRENERGIC RECEPTORS, Brain research, 659(1-2), 1994, pp. 208-212
The goal of this study was to determine whether diabetes mellitus alte
rs reactivity of the basilar artery in vivo to activation of beta-adre
nergic receptors. We measured diameter of the basilar artery in non-di
abetic and diabetic (streptozotocin 50-60 mg/kg i.p.) rats during supe
rfusion with isoproterenol and norepinephrine, which dilate cerebral b
lood vessels via activation of beta-adrenergic receptors. Dilatation o
f the basilar artery in response to isoproterenol and norepinephrine w
as significantly less in diabetic compared to non-diabetic rats. To de
termine 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 di
latation of the basilar artery in response to forskolin, a direct acti
vator of adenylate cyclase. In contrast to that observed for isoproter
enol and norepinephrine, forskolin produced similar dilatation of the
basilar artery in non-diabetic and diabetic rats. Thus, the findings o
f the present study suggest that diabetes mellitus impairs dilatation
of the basilar artery in vivo in response to activation of beta-adrene
rgic receptors. In addition, impairment of beta-adrenergic mediated di
latation of the basilar artery during diabetes mellitus does not appea
r to be related to an alteration in catalytic activity of adenylate cy
clase.