One of the receptor-mediated events, cyclic nucleotide, i.e. cAMP and cGMP formation induced by bradykinin in guinea pig ileum was investigated in this report. Bradykinin, similar to acetylcholine, produced a rapid rise in the levels of cAMP and cGMP in the ileum. The absolute amount of these cyclic nucleotides induced by the same dosages (10(-8) to 10(-6) M) of bradykinin was greater in cAMP than in cGMP. This increase in cyclic nucleotides was dependent upon the presence of calcium in the medium. Addition of EGTA (0.1 mM) in a calcium free medium resulted in a significant reduction of the levels. The elevation of cAMP and cGMP levels induced by bradykinin in the ileum could not be blocked by either atropine (an anticholinergic agent) or propranolol (a beta-adrenergic blocker). Both of these blockers did not alter the basal levels of two cyclic nucleotides. However bradykinin-induced cAMP formation could be completely blocked by either indomethacin (a prostaglandin synthesis inhibitor) or dexamethasone (a phospholipase A2 inhibitor), This, however, was not true in the case of bradykinin induced cGMP formation. Additionally, both blockers did not create a significant change in the basal levels of these cyclic nucleotides. Bradykinin induced cAMP formation in the ileum was indicated by observed results to likely occur through an indirect process, i.e. the formation and release of prostaglandin in the cell, whereas bradykinin-induced cGMP formation did not. The elevation of these cyclic nucleotides in the cells was observed to be related to the movement of calcium ion across the cell membrane.