Article date: January 2000
By: Anthie Ellis, Chun Guang Li, Michael J Rand, in Volume 129, Issue 2, pages 315-322
The effects of L‐cysteine were tested in rat aortic rings on responses to nitric oxide free radical (NO•), nitroxyl (NO−) derived from Angeli's salt and endothelium‐derived relaxing factor (EDRF) activated by acetylcholine, ATP and the calcium ionophore A23187. Concentrations of 300 μM or less of L‐cysteine had no effect on responses.
Relaxations produced by exogenous NO• (0.25–2.5 μM) were markedly prolonged and relaxations produced by sodium nitroprusside (0.001–0.3 μM) were enhanced by 1 and 3 mML‐cysteine. The enhancements by L‐cysteine of responses to NO• and sodium nitroprusside may be attributed to the formation of S‐nitrosocysteine.
Relaxations mediated by the nitroxyl anion (0.3 μM) donated from Angeli's salt were more prolonged than those produced by NO•, and nitroxyl‐induced relaxations were reduced by L‐cysteine (1 and 3 mM).
EDRF‐mediated relaxations produced by acetylcholine (0.01–10 μM), ATP (3–100 μM) and the calcium ionophore A23187 (0.1 μM) were significantly reduced by 3 mML‐cysteine.
The similarity between the inhibitory effects of L‐cysteine on responses to EDRF and on those to nitroxyl suggests that a component of the response to EDRF may be mediated by nitroxyl anion.
The effects of L‐cysteine were tested in rat aortic rings on responses to nitric oxide free radical (NO•), nitroxyl (NO−) derived from Angeli's salt and endothelium‐derived relaxing factor (EDRF) activated by acetylcholine, ATP and the calcium ionophore A23187. Concentrations of 300 μM or less of L‐cysteine had no effect on responses.
Relaxations produced by exogenous NO• (0.25–2.5 μM) were markedly prolonged and relaxations produced by sodium nitroprusside (0.001–0.3 μM) were enhanced by 1 and 3 mML‐cysteine. The enhancements by L‐cysteine of responses to NO• and sodium nitroprusside may be attributed to the formation of S‐nitrosocysteine.
Relaxations mediated by the nitroxyl anion (0.3 μM) donated from Angeli's salt were more prolonged than those produced by NO•, and nitroxyl‐induced relaxations were reduced by L‐cysteine (1 and 3 mM).
EDRF‐mediated relaxations produced by acetylcholine (0.01–10 μM), ATP (3–100 μM) and the calcium ionophore A23187 (0.1 μM) were significantly reduced by 3 mML‐cysteine.
The similarity between the inhibitory effects of L‐cysteine on responses to EDRF and on those to nitroxyl suggests that a component of the response to EDRF may be mediated by nitroxyl anion.
British Journal of Pharmacology (2000) 129, 315–322; doi:10.1038/sj.bjp.0703058
DOI: 10.1038/sj.bjp.0703058
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