Activation of the adrenergic beta-receptor stimulates prolactin release from primary cultured pituitary cells

Prolactin release from primary cultured pituitary cells was investigated using a dynamic perifusion system. Although epinephrine (1 mumol/l) produced an elevation in the mean value of the prolactin concentration at the onset of the perifusion, the elevation was not statistically significant, and the overall effect of the epinephrine was to produce an inhibition of prolactin release. The alpha- and D2-receptors of the primary cultured cells were functionally removed by a pretreatment with phenoxybenzamine (0.1 or 1 mumol/l). Since phenoxybenzamine irreversibly inactivates both the adrenergic alpha- and the D2-receptors but does not block the beta-receptors, the enhanced stimulatory action of the epinephrine (1 mumol/l) on the phenoxybenzamine pretreated cells suggests the involvement of adrenergic beta-receptors in prolactin release. Perifusion of isoproterenol (1 mumol/l), a beta-receptor agonist, stimulated prolactin release. This stimulation was blocked by beta-receptor antagonism with propranolol (1 mumol/l) supporting the implication of the beta-receptor in prolactin release. In order to differentiate between beta 1- and beta 2-receptor involvement, we investigated the effects of ICI 118,551 (1 mumol/l) on isoproterenol-induced prolactin release. ICI 118,551, a selective beta 2-receptor antagonist, blocked the stimulatory action of isoproterenol on prolactin release indicating that the beta-receptor responsible for the stimulation of prolactin release belongs to the beta 2-receptor family. Moreover, the demonstration that salbutamol, a selective beta 2-receptor agonist, stimulated prolactin secretion offers further evidence in support of the role of the beta 2-receptor in the stimulation of prolactin release.(ABSTRACT TRUNCATED AT 250 WORDS)