Inhibition of L-arginine transport by reactive oxygen species in rat anococcygeus muscle

Durlu N. T. , Ismailoglu U. , Sahin-Erdemli I.

FUNDAMENTAL & CLINICAL PHARMACOLOGY, vol.17, no.5, pp.609-614, 2003 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 17 Issue: 5
  • Publication Date: 2003
  • Doi Number: 10.1046/j.1472-8206.2003.00184.x
  • Page Numbers: pp.609-614


The effect of L-arginine on nitrergic transmission and its alteration with reactive oxygen species (ROS) were investigated. L-arginine potentiated the relaxation response induced by electrical field stimulation in rat anococygeus muscle. This effect was inhibited by L-lysine, a cationic amino acid using y(+)L and y(+) transport systems in a similar way with L-arginine. The neutral amino acid L-leucine, which uses only y(+)L system as a transport mechanism, inhibited this potentiation at only low frequency stimulation. Electrolysis of the physiological solution did not change the responses to electrical field stimulation, but inhibited the potentiation elicited by L-arginine that was prevented in the presence of mannitol and N-acetyl-L-cysteine. In conclusion, L-arginine is transported via y(+) system predominantly to potentiate the relaxation response to nitrergic nerve stimulation in rat anococcygeus muscle. ROS, primarily hydroxyl radicals inhibited L-arginine-induced potentiation probably by interacting with the y(+) amino acid transport system.