The presence of kallikrein activity, bradykinin (BK) and lys-bradykinin (LBK) in the pituitary gland suggests a possible physiological role of kinins therein. We demonstrated that BK and LBK increased prolactin (PRL), but not growth hormone release, from rat anterior pituitary cells cultured in vitro. Such stimulatory effect on PRL secretion appears to involve B2-type BK receptors, as suggested by the antagonizing effect of B6572 (a B2-type BK receptor antagonist) on PRL release. The BK-induced increase in PRL release is associated with an enhanced [3H]arachidonate (AA) efflux, an elevated cytosolic free calcium concentration [(Ca2+]i), and increased inositol phosphate (InsPx) production. Bradykinin and LBK stimulated [3H]AA liberation, [Ca2+]i elevation and PRL release at lower concentrations than those necessary to stimulate InsPx production. Therefore, AA release and [Ca2+]i elevation may be more important to PRL release than is InsPx production. Dopamine (DA) inhibited BK- or LBK-stimulated PRL release and slightly attenuated the stimulated [Ca2+]i response, but had no effect on stimulated [3H]AA efflux and InsPx generation. This study suggests that BK and LBK may have either an autocrine or a paracrine role in regulating PRL secretion, and are subject to modulation by DA.