Cysteine Hydrochloride

L-Cysteine hydrochloride produced concentration-dependent opposite effects on vascular relaxations mediated by nitric oxide and nitroxyl anion in rat aortic rings. At millimolar concentrations, L-cysteine markedly prolonged relaxations induced by exogenous nitric oxide free radical and enhanced responses to sodium nitroprusside, an effect attributed to the formation of S-nitrosocysteine which acts as a nitric oxide carrier molecule. In contrast, the same concentrations of L-cysteine significantly reduced endothelium-derived relaxing factor-mediated relaxations produced by acetylcholine, ATP and the calcium ionophore A23187.
L-Cysteine also reduced relaxations induced by the nitroxyl anion donated from Angeli's salt. The similarity between the inhibitory effects of L-cysteine on responses to EDRF and on those to nitroxyl anion suggested that a component of EDRF-mediated relaxation may be mediated by nitroxyl anion rather than nitric oxide free radical alone. L-Cysteine hydrochloride and L-cysteine free base showed differential direct effects on vascular tension during sustained relaxations, with the hydrochloride salt producing a biphasic response consisting of an initial short-lasting relaxation followed by a slowly developing contraction, while the free base produced only contraction.

Fig. 1 Effects of L-cysteine on vasorelaxation. (Ellis A.; et al. 2000)