Increase of nitric oxide by L-arginine potentiates beta-endorphin- but not mu-, delta- or kappa-opioid agonist-induced antinociception in the mouse.

L-Arginine pretreated i.c.v. produced a time- and dose-dependent potentiation of beta-endorphin-induced inhibition of the tail-flick response in ICR mice. However, the inhibition of the tail-flick response induced by morphine, DAMGO ([D-Ala2,NMePhe4,Gly5-ol]enkephalin), DPDPE ([D-Pen2,D-Pen5]enkephalin or U50,488H given i.c.v. was not potentiated by i.c.v. pretreated L-arginine. The results indicate that L-arginine selectively potentiates antinociception induced by epsilon-opioid receptor agonist, but not mu-, delta- or kappa-opioid receptor agonist. L-Arginine pretreated i.t. did not potentiate i.c.v. administered beta-endorphin-induced inhibition of the tail-flick response, indicating that the potentiating effect of L-arginine on beta-endorphin-induced antinociception is located at the supraspinal sites but not at the spinal sites.