@article{oai:nagasaki-u.repo.nii.ac.jp:00001580,
 author = {KANETO, Hiroshi and TAKAHASHI, Masakatsu and WATANABE, Joe},
 issue = {7},
 journal = {Journal of Pharmacobio-Dynamics},
 month = {},
 note = {Differences of affinity ot and selectivity for trimebutine between peripheral and central opioid receptors have been investigated. Trimebutine inhibited electrically induced contraction of guinea-pig ileum (GPI) and mouse vas deferens (MVD) but not of rabbit vas deferens, and the inhibition was antagonized by naloxone and, to lesser extent, by nor-binaltorphimine (nor-BNI). The pA2 values for morphine and trimebutine with naloxone were higher than the values for these compounds with nor-BNI in both GPI and MVD preparations. GPI preparations incubated with a high concentration of morphine or trimebutine developed tolerance ; however, there was no cross-tolerance between them, suggesting difference in the underlying mechanisms. In mouse and guinea-pig brain homogenate trimebutine was about 1/13 as potent as morphine to displace the [3H]naloxone binding, while it has no appreciable affinity for κ-opioid receptors in [3H]U-69593, a selective κ-receptor agonist. These results suggest that trimebutine, showing its low affinity to opioid receptors, possesses μ-receptor selective properties rather than those of κ-opioid receptor in the peripheral tissues and in the central brain homogenate., Journal of Pharmacobio-Dynamics, 13(7), pp.448-453; 1990},
 pages = {448--453},
 title = {The opioid receptor selectivity for trimebutine in isolated tissues experiments and receptor binding studies.},
 volume = {13},
 year = {1990}
}