Selective inhibition of the inducible nitric oxide synthase by aminoguanidine.

Abstract

Overproduction of the free radical nitric oxide (NO) has been implicated in the pathogenesis of a variety of inflammatory and immunologically mediated diseases as well as complications of diabetes. In the present study we have demonstrated that aminoguanidine selectively inhibits the cytokine-inducible isoform of NO synthase which appears to be responsible for the excess production of NO linked to these disease states. By using organ, cell, and enzyme-based measurements we have shown that aminoguanidine is equipotent to NG-monomethyl-L-arginine (L-NMA) as an inhibitor of the cytokine-induced isoform of NO synthase but is 10 to 100-fold less potent as an inhibitor of the constitutive isoform. Thus, aminoguanidine may be useful as a selective inhibitor of the inducible NO synthase in the treatment of disease states characterized by the pathological overproduction of NO.

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@article{Misko1993SelectiveIO, title={Selective inhibition of the inducible nitric oxide synthase by aminoguanidine.}, author={Thomas P. Misko and William M. Moore and Thomas P. Kasten and G. Allen Nickols and John Corbett and Ronald G . Tilton and Michael L. McDaniel and Jamie R. Williamson and Mark G. Currie}, journal={European journal of pharmacology}, year={1993}, volume={233 1}, pages={119-25} }