The enhancing effects of peptidase inhibitors on the antinociceptive action of 〔Met[5]〕enkephalin-Arg[6]-Phe[7] in rats

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  • Takahashi Shigeru
    Department of Clinical Pharmacology, School of Medicine, Tokai University, Japan
  • Jin Xing Lu
    Department of Clinical Pharmacology, School of Medicine, Tokai University, Japan
  • Kosaka Kenya
    Department of Clinical Pharmacology, School of Medicine, Tokai University, Japan
  • Yoshikawa Masanobu
    Department of Clinical Pharmacology, School of Medicine, Tokai University, Japan
  • Kobayashi Hiroyuki
    Department of Clinical Pharmacology, School of Medicine, Tokai University, Japan
  • Oka Tetsuo
    Department of Clinical Pharmacology, School of Medicine, Tokai University, Japan

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  • The Enhancing Effects of Peptidase Inhibitors on the Antinociceptive Action of [Met5]Enkephalin-Arg6-Phe7 in Rats

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Previous in vitro studies have shown that the degradation of [Met5]enkephalin-Arg6-Phe7 during incubation with cerebral membrane preparations is largely prevented by a mixture of three peptidase inhibitors: amastatin, captopril, and phosphoramidon. The present in vivo study shows that the inhibitory effect of [Met5]enkephalin-Arg6-Phe7 administered intra-third-ventricularly on the tail-flick response was increased more than 1000-fold by the intra-third-ventricular pretreatment with three peptidase inhibitors. The antinociceptive effect produced by the [Met5]enkephalin-Arg6-Phe7 in rats pretreated with any combination of two peptidase inhibitors was significantly smaller than that in rats pretreated with three peptidase inhibitors, indicating that any residual single peptidase could inactivate significant amounts of the [Met5]enkephalin-Arg6-Phe7. The present data, together with those obtained from previous studies, clearly show that amastatin-, captopril-, and phosphoramidon-sensitive enzymes play important roles in the inactivation of endogenous opioid peptides, such as [Met5]enkephalin, [Met5]enkephalin-Arg6-Phe7, [Met5]enkephalin-Arg6-Gly7-Leu8, and dynorphin A (1-8), administered intra-third-ventricularly to rats.<br>

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