Increase of nitric oxide production by L-arginine potentiates i.c.v. administered beta-endorphin-induced antinociception in the mouse.
Pretreatment (i.c.v.) of mice with L-arginine but not D-arginine potentiated beta-endorphin-induced (i.c.v. administered) inhibition of the tail-flick response. The potentiation was attenuated by N omega-nitro-L-arginine methyl ester, a selective inhibitor of nitric oxide synthase. This observation suggests that increased production of nitric oxide from L-arginine mediates the potentiation of beta-endorphin-induced antinociception.
Tseng
L F
LF
Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee 53226.
Xu
J Y
JY
Pieper
G M
GM
D000594:Amino Acid Oxidoreductases / Q000037:antagonists & inhibitors; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D004357:Drug Synergism; D007276:Injections, Intraventricular; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D019331:NG-Nitroarginine Methyl Ester; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase; D010146:Pain / Q000378:metabolism*; D001615:beta-Endorphin / Q000494:pharmacology*
D009569:Nitric Oxide; D001615:beta-Endorphin; D001120:Arginine; D019001:Nitric Oxide Synthase; D000594:Amino Acid Oxidoreductases; D019331:NG-Nitroarginine Methyl Ester