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Inhibition of l‐ arginine transport by reactive oxygen species in rat anococcygeus muscle
Author(s) -
Tugba Durlu N.,
Burcin Ismailoglu U.,
SahinErdemli Inci
Publication year - 2003
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1046/j.1472-8206.2003.00184.x
Subject(s) - arginine , stimulation , chemistry , long term potentiation , amino acid , biochemistry , cysteine , reactive oxygen species , biophysics , biology , endocrinology , enzyme , receptor
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.