Facilitation of norepinephrine release from cerebral cortex is mediated by beta 2-adrenergic receptors

Facilitatory effects of prenalterol and albuterol (beta 1- and beta 2-selective adrenergic agonists, respectively) in the absence and presence of propranolol (a nonselective beta-adrenergic antagonist), ICI 89,406 or ICI 118,551 (beta 1- and beta 2-selective adrenergic antagonists, respectively) on electrical stimulation-evoked release of 3H-NE from rat cerebral cortical slices were assessed. Albuterol (0.1-100 nM) increased evoked release of 3H-NE from the cerebral cortical slices with greater potency than prenalterol (1-100 nM). The beta 2-adrenergic antagonist ICI 118,551 (1 nM) and propranolol (50 nM) abolished the facilitatory effects of albuterol (0.1 and 10 nM). In contrast, the beta 1-adrenergic antagonist ICI 89,406 (1 nM) did not alter the release-enhancing effect of albuterol. Prenalterol (10 and 100 nM)-induced facilitation of evoked release of 3H-NE was abolished by ICI 118,551; propranolol reduced the effect of 10 nM prenalterol and abolished that of 100 nM prenalterol. ICI 89,406 inhibited the effect of 100 nM prenalterol without altering that of 10 nM prenalterol. Basal release of 3H-NE was not altered by the drugs used in this study. These results suggest that facilitation of 3H-NE release induced by beta-adrenergic agonists is mediated primarily by beta 2-adrenergic receptors.