| The aim of present studies was to investigate the interactions between endokinin A/B(EKA/B),endokinin C/D(EKC/D)and endomorphin-1(EM-1)on the depressor effect and mechanisms at peripheral level.EKA/B at low concentrations caused hyperalgesia significantly;hemopressin(HP)could revert the hyperalgesia induced by either carrageenan or bradykinin,and also by spinal cord injury.Investigate the effects and mechanisms of antinociceptive action regulation of HP in brain levels to EKA/B and EKC/D.The depressor effects of EKA/B produced a U-shaped curve.The maximal effect was caused by the dose of 10 nmol/kg.The depressor effect of EKC/D and EM-1 showed dose-dependent relationships.Co-administration of EKA/B,EM-1 or EKC/D + EM-1 produced effects similar to those of EKA/B alone.Co-administration of EKC/D with EM-1 caused a dose-dependent depressor effect.SR140333B,SR48968C,SR142801,naloxone and NG-nitro-l-arginine methyl ester(L-NAME)were used to investigate mechanisms.HP(10 nmol,1 nmol,100 pmol,10 pmol,5 pmol)could fully inverted the hyperalgesia induced by EKA/B(10,30,100 pmol),and showed antinociception.HP(less than 1 pmol)could not block the hyperalgesia induce by EKA/B(30 pmol).HP(10 pmol,100 pmol,1 nmol)could block the antinociception induced by EKA/B(3 nmol)and extend the duration of the strongest analgesic;HP(1 nmol,100 pmol,10 pmol)could extend the peak duration induced by EKC/D(3 nmol)changed to partially block the analgesic of EKC/D(3 nmol).HP(less than 10 pmol)could strengthen the analgesic of EKC/D(3 nmol).It has a secondary peak at 50 min after administration.SR140333B,SR142801 were used to mechanism studies.This study describes the effects of EKA/B,EKC/D,and EM-1 on the regulation of MAP in rats and antinociceptive action regulation of HP in brain levels to EKA/B and EKC/D.The results in our study may provide some evidence for the further study of tachykinins and tachykinin-like peptide in mean arterial blood pressure,antagonized hyperalgesia and prolonged analgesia. |
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