Prolactin (Prl) responses to anesthetics, stress of immobilization, and agents that block adrenergic receptors were determined in 13 female rhesus monkeys. The local anesthetic (lidocaine HC1) had no effect, but the general anesthetics (ketamine HC1 and sodium pentobarbital) significantly increased serum Prl levels in intact animals. There was no indication of a pentobarbital-induced inhibition of Prl secretion as reported for other species. A combination of halothane anesthesia and immobilization for 30 or 60 min produced significantly greater increases in Prl levels than immobilization alone for similar periods of time. Prl responses to blockers of adrenergic receptors varied in chair-adapted ovariectomized monkeys. The increase in serum Prl concentrations produced by the β-receptor blocker propranolol was less marked than that induced by the α-receptor blockers phentolamine and phenoxybenzamine. Prl elevations of the highest magnitude and longest duration were produced by haloperidol, which blocks both adrenergic and dopaminergic receptors. Pretreatment of these animals with estradio1-17β had no effect on Prl responses to phentolamine and haloperidol. These results indicate involvement of an adrenergic neurotransmitter system in the control of Prl secretion in primat