Selective inhibition of the inducible nitric oxide synthase by aminoguanidine

Thomas P. Misko, William M. Moore, Thomas P. Kasten, G. Allen Nickols, John A. Corbett, Ronald G. Tilton, Michael L. McDaniel, Joseph R. Williamson, Mark G. Currie

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715 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)119-125
Number of pages7
JournalEuropean Journal of Pharmacology
Issue number1
StatePublished - Mar 16 1993
Externally publishedYes


  • Aminoguanidine
  • Nitric oxide synthase
  • Selective inhibitor inducible

ASJC Scopus subject areas

  • Pharmacology


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