Clinical data indicate that the control of gastrin secretion from the human antrum has a beta-adrenergic component. The purpose of the present study was to investigate whether this was due to the presence of beta-adrenergic receptors on the G cells. A newly developed short-term culture system of enriched antral G cells was used to eliminate the possibility of input from factors in the circulation and the peripheral innervation. The results demonstrated that epinephrine and terbutaline (a beta 2 agonist) significantly stimulated gastrin release above basal which could be blocked by the addition of propranolol (beta-adrenergic antagonist). However, the beta 1 agonist, dobutamine, and phenylepinephrine did not stimulate gastrin release above basal. In addition, simultaneous administration of epinephrine and the neuropeptide, bombesin, resulted in a potentiation of gastrin release. It was concluded that the stimulatory effect of the sympathetic system on gastrin release was mediated through beta 2-adrenergic receptors. The data indicated that adrenaline released from the adrenal medulla and gastrin releasing peptide (the mammalian homolog of bombesin) released from the intrinsic innervation of the stomach interact with respect to the stimulation of gastrin.