The analgesic and respiratory depressant actions of metorphamide in mice and rabbits

• Published in: Neuropeptides (Edinburgh) Vol. 6; no. 2; pp. 121 - 131
• Main Authors: Xu, ShaoFen, Lu, WenXiao, Zhou, KaiRong, He, XiaoPin, Niu, ShanFu, Xu, WeiMin, Zhang, AnZhong, Weber, E., Chang, J.K.
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 01.01.1985; Elsevier
• Subjects: Analgesics; Animals; Biological and medical sciences; Depression, Chemical; Enkephalin, Methionine - analogs & derivatives; Enkephalin, Methionine - antagonists & inhibitors; Enkephalin, Methionine - pharmacology; Female; Injections, Intraventricular; Male; Medical sciences; Mice; Naloxone - analogs & derivatives; Naloxone - pharmacology; Neuropharmacology; Pharmacology. Drug treatments; Rabbits; Respiration - drug effects; Sensory Thresholds; Rodentia; Rabbit; Brain (Vertebrata); Lagomorpha; Neuropeptide; Opioid peptide; Opiate receptor μ; Biological activity; Analgesia; Vertebrata; Mammalia; Mouse; Animal; Affinity; Respiration
• ISSN: 0143-4179; 1532-2785
• DOI: 10.1016/0143-4179(85)90103-9

Metorphamide (MET) elicited a potent, dose-dependent analgesia and respiratory depression in mice and rabbits. MET induced-analgesia was naloxone reversible and potentiated by bestatin. Naloxonazine, a relatively selective mu 1 blocker, at certain dosage (50 μg per rabbit, icv), could abolish the analgesia but not the respiratory inhibition produced by MET. Our result indicates that mu 1 receptors mediate the MET induced-analgesia but not its respiratory effect. Since MET is a mu- and kappa-ligand with very low delta activity, the MET induced respiratory depression may be mediated by mu 2 or kappa binding sites.