Abstract
The pharmacological effects of naloxone on cerebral arterial smooth muscle in vitro were examined using canine basilar arterial strips. Naloxone exerted two different effects on canine basilar artery: (1) at a high concentration (3 × 10−4 M) it produced nonspecific vasodilation, and (2) at lower concentrations (3 × 10−7, 3 × 10−6, and 3 × 10−5 M) it inhibited the vasoconstrictor effects of norepinephrine without altering KCl-, serotonin-, or hemoglobin-induced constriction. Morphine (2 × 10−5 or 2 × 10−4 M) did not reverse the specific vasodilating effect of naloxone (3 × 10−5 M) on norepinephrine-induced constriction. Rather, morphine and naloxone together produced a greater vasodilating effect on norepinephrine-induced constriction than either agent alone. Naloxone (3 × 10−5M) failed to alter either phenylephrine-induced constriction or clonidine-induced constriction. The vasodilating effect of naloxone (3 × 10−5 M) on 10−3 M norepinephrine-induced constriction was not reduced with 10−6 M propranolol. These results suggest that the vasodilating effect of naloxone on norepinephrine-induced constriction does not result from an antagonistic action on opiate receptors, direct inhibition of α-adrenoreceptors, or direct stimulation of β-adrenoreceptors in canine cerebral arterial smooth muscle. The vasodilating effect of naloxone on norepinephrine-induced constriction may influence the CBF changes following naloxone administration.