The Inactivation of [Met5]-Enkephalin by Bestatin-Sensitive Aminopeptidase, Captopril-Sensitive Peptidyl Dipeptidase A and Thiorphan-Sensitive Endopeptidase-24.11 in Mouse Vas Deferens

Aoki, Kazuko; Kajiwara, Midori; Oka, Tetsuo

doi:10.1254/jjp.40.297

Cited by 28 publications

(11 citation statements)

References 12 publications

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“…Mouse vas deferens was harvested and prepared for electrical stimulation as described previously [24]. The percent (%) inhibition of stimulated muscle twitch produced by each opioid was plotted against its log concentration to determine the IC 50 (concentration required to produce 50% inhibition of the twitch).…”

Section: In Vitro Isolated Preparationsmentioning

confidence: 99%

Effect of Peptidase Inhibitors on Dynorphin A (1-17) or (1-13)-Induced Antinociception and Toxicity at Spinal Level

Matsuda¹,

Yoshikawa²,

Kan³

et al. 2017

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Our group has earlier demonstrated that three enzymes sensitive to peptidase inhibitors (PIs), amastatin (A)-, captopril (C)-, and phosphoramidon (P), played an important role in inactivation of enkephalins at the spinal level. Dynorphin-converting enzyme (DCE) hydrolyzes dynorphin (Dyn) A (1-17) or Dyn A (1-13) mainly at the Arg 6 -Arg 7 bond. Dynorphin A and its derived peptides interact with opioid and glutamate receptors at their N-and C-terminals, respectively. The purpose of the present study was to evaluate the antinociceptive potency and toxicity of intrathecal administered Dyn A (1-17), Dyn A (1-13), or Dyn A (1-6) under pretreatment with ACP and/or the DCE inhibitor p-hydroxymercuribenzoate (PHMB). The effect of these PIs on Dyn A (1-17)-induced inhibition of electrically-evoked contractions in mouse vas deferens was also investigated. The inhibitory potency of Dyn A (1-17) on electrically-evoked contractions in mouse vas deferens under pretreatment with ACP was higher than that with AC, AP, or CP. Pretreatment with ACP augmented Dyn A (1-17) or (1-13)-induced antinociception by approximately 50-or 30-fold with no sign of allodynia when administered intrathecally at low doses. Pretreatment with ACP and PHMB induced neuropathy. These findings showed that intrathecal administration of low-dose Dyn A (1-17) or DynA (1-13) increased antinociception under pretreatment with ACP, but without signs of allodynia in rat.

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Section: In Vitro Isolated Preparationsmentioning

confidence: 99%

Effect of Peptidase Inhibitors on Dynorphin A (1-17) or (1-13)-Induced Antinociception and Toxicity at Spinal Level

Matsuda¹,

Yoshikawa²,

Kan³

et al. 2017

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“…A mixture of an aminopeptidase inhibitor, a peptidyl dipeptidase A inhibitor and an enkephalinase inhibitor has been shown to completely protect Met-enk from degradation produced by incubation with either an ileal or a striatal membrane fraction from guinea pigs (15). Also, it has been shown that the effects of Met-enk in vivo and in vitro were potentiated by the mixture of peptidase inhibitors; the loss of the righting reflex and the inhibition of the tail-flick response were produced by Met-enk ad ministered s.c. in infant rats pretreated with the mixture of three peptidase inhibitors (16), and the inhibitory effect of Met-enk on the contraction of isolated ileum (17,18) and vas deferens (17,19,20) were increased by the mix ture of peptidase inhibitors. However, the enzymatic degradation of p-end and Dyn is not fully understood, and the involvement of the Met-enk hydrolyzing enzymes in the degradation of A-end and Dyn in CNS is not clear.…”

Section: Introductionmentioning

confidence: 96%

Effects of a Mixture of Peptidase Inhibitors (Amastatin, Captopril and Phosphoramidon) on Met-Enkephalin-, β-Endorphin-, Dynorphin-(l-13)- and Electroacupuncture-Induced Antinociception in Rats

Kishioka¹,

Miyamoto²,

Fukunaga³

et al. 1994

Japanese Journal of Pharmacology

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ABSTRACT-The effects of a mixture of three peptidase inhibitors (PIs), amastatin, captopril and phosphoramidon, on methionine-enkephalin (Met-enk)-, j3-endorphin (p-end)-, dynorphin-(1 13) (Dyn) and electroacupuncture (EA)-induced antinociception were compared in rats. EA was performed by passing electric pulses (3 Hz, 0.1-msec duration, for 45 min) through acupuncture needles inserted into the Hoku point. The antinociceptive effect was estimated by the hind paw pressure test. The antinociceptive effects of Met-enk and p-end injected i.c.v. or Lt. and of Dyn injected i.t. were clearly potentiated by the PIs pretreated by the same administration routes as used for the injection of opioid peptides. The antinocicep tive effects of Met-enk, n-end and Dyn injected i.c.v. were also potentiated significantly by i.t.-PIs. PIs in jected into the periaqueductal gray (PAG) potentiated EA antinociception. However, the EA effect was not affected by i.t.-PIs and was rather attenuated by i.c.v.-PIs. These results suggest that: i) Met-enk hydro lyzing enzymes are involved in the degradation of not only Met-enk but also p-end and Dyn in the rat central nervous system; ii) Met-enk and n-end act on both supraspinal and spinal sites, while Dyn acts only on the spinal site; iii) EA antinociception is mediated by supraspinal Met-enk and/or n-end; and iv) an anti-opiate peptide system may be activated by EA stimulation, being susceptible to Met-enk hydrolyzing enzymes.

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Section: Deferensmentioning

confidence: 99%

“…11 ("enkephalinase", EC 3.4.24.11), and captopril-sensitive peptidyl dipeptidase A (angiotensin I converting enzyme, kininase II, peptidyldipeptide hy drolase, EC 3.4.15.1), have been shown to play important roles in the inactivation of exogenously given enkephalin in two in vitro isolated preparations, guinea-pig ileum (1) and mouse vas deferens (2). Additionally, these three enzymes have been indicated to be located very close to opioid receptors (1,2). Moreover, enkephalin has been shown to be exclusively inactivated by these three peptidases, since enkephalin remains intact almost totally after it is incubated with either ileal or striatal membrane fractions of guinea pig for 60 min at 37'C in the presence of three peptidase inhibitors, amastatin, thior phan and captopril, although free tyrosine and the Tyr-Gly-Gly fragment are produced when the incubation mixture does not contain the peptidase inhibitor (3).…”

Section: Deferensmentioning

confidence: 99%

“…When the effect of peptidase inhibitors on the IC50 value of [Met5]-enkephalin was studied, they were given at least ten minutes before the enkephalin administration. The % difference shown in the table was calculated as described previously (2). The significance of % differences between IC50 values of two adjacent groups shown in the table was determined by the paired Student's t-test.…”

Section: Chemicalsmentioning

confidence: 99%

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The Enhancing Effects of Amastatin, Phosphoramidon and Captopril on the Potency of [Met5]-Enkephal n in Rat Vas Deferens

Cui

Kajiwara

Ishii

et al. 1986

Japanese Journal of Pharmacology

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The Inactivation of [Met5]-Enkephalin by Bestatin-Sensitive Aminopeptidase, Captopril-Sensitive Peptidyl Dipeptidase A and Thiorphan-Sensitive Endopeptidase-24.11 in Mouse Vas Deferens

Cited by 28 publications

References 12 publications

Effect of Peptidase Inhibitors on Dynorphin A (1-17) or (1-13)-Induced Antinociception and Toxicity at Spinal Level

Effect of Peptidase Inhibitors on Dynorphin A (1-17) or (1-13)-Induced Antinociception and Toxicity at Spinal Level

Effects of a Mixture of Peptidase Inhibitors (Amastatin, Captopril and Phosphoramidon) on Met-Enkephalin-, β-Endorphin-, Dynorphin-(l-13)- and Electroacupuncture-Induced Antinociception in Rats

The Enhancing Effects of Amastatin, Phosphoramidon and Captopril on the Potency of [Met5]-Enkephal n in Rat Vas Deferens

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