Why the study?
Does L-cysteine alter the relaxation responses to nitric oxide, nitroxyl anions, and EDRF in rat aortic rings?
Does L-cysteine alter the relaxation responses to nitric oxide, nitroxyl anions, and EDRF in rat aortic rings?
The similarity in inhibitory effects of L-cysteine on responses to EDRF and nitroxyl suggests that a component of the EDRF response may be mediated by nitroxyl anion.
Answers are grounded in this paper and cite their sources.
Supports nitroxyl as possible EDRF component; hypothesis-generating for vascular NO signaling and precludes clinical translation.
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 microM or less of L-cysteine had no effect on responses. 2. Relaxations produced by exogenous NO(*) (0.25 - 2.5 microM) were markedly prolonged and relaxations produced by sodium nitroprusside (0.001 - 0.3 microM) were enhanced by 1 and 3 mM L-cysteine. The enhancements by L-cysteine of responses to NO(*) and sodium nitroprusside may be attributed to the formation of S-nitrosocysteine. 3. Relaxations mediated by the nitroxyl anion (0.3 microM) 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). 4. EDRF-mediated relaxations produced by acetylcholine (0.01 - 10 microM), ATP (3 - 100 microM) and the calcium ionophore A23187 (0.1 microM) were significantly reduced by 3 mM L-cysteine. 5. The similarity between the inhibitory effects of L-cystei on responses to EDRF and on those to nitroxyl suggests that a component of the response to EDRF may be mediated by nitroxyl anion.
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Ellis et al. (2000) studied this question.
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