The purpose of this study was to investigate the differential involvement of distinct types of opioid receptors in the modulation of intestinal peristalsis compared to electrically induced longitudinal muscle contractions. Like naloxone, the proposed sigma-agonist and mu-antagonist SKF 10,047 (N-allyl-normetazocine) dose-dependently enhanced peristaltic circular muscle contractions in the isolated guinea-pig ileum. Pre-application of SKF 10,047 at a concentration which itself enhanced peristalsis by 20% on average strongly attenuated the inhibition of peristalsis produced by opioids previously proposed to act via mu-opioid-receptors in the guinea-pig ileum, i.e. normorphine, beta-endorphin, D-Ala2-D-Leu5-enkephalin and d-Ser2-L-Leu5-enkephalyl-Thr, but less strongly attenuated the inhibition produced by compounds suggested to act via kappa-opioid-receptors in this tissue, i.e. ethylketazocine and dynorphin (1-13). In contrast to its effect on peristalsis, SKF 10,047 inhibited the electrically induced contractions of the myenteric plexus-longitudinal muscle preparation in a naloxone-reversible fashion. It may be concluded that mu-and kappa-opioid receptors are of a greater functional significance than sigma-receptors in the control of peristalsis. sigma-Receptors might participate predominantly in modulating the release of acetylcholine which underlies the electrically induced longitudinal muscle contraction.