Urinary nitrate excretion in relation to murine macrophage activation. Influence of dietary L-arginine and oral NG-monomethyl-L-arginine.
 Murine macrophage oxidation of L-arginine guanidino nitrogen to nitrite/nitrate yields an intermediate effector, possibly nitric oxide, with antimicrobial activity.
 Total body nitrogen oxidation metabolism (NOM) was measured in vivo by determining the urinary nitrate excretion of mice ingesting a chemically defined nitrite/nitrate-free diet.
 As reported previously, mycobacterial infection with bacillus Calmette-Guerin led to a large increase in urinary nitrate excretion.
 This increase was temporally related to macrophage activation in vivo.
 The substrate for macrophage nitrogen oxidation metabolism in vitro, L-arginine, was deleted from the diet without ameliorating the urinary nitrate excretion response induced by BCG.
 This suggested that L-arginine was synthesized endogenously because there are no other known natural substrates for NOM.
 A competitive inhibitor of NOM, the L-arginine analog, NG-monomethyl-L-arginine was fed to mice in their drinking water.
 NG-monomethyl-L-arginine ingestion blocked both basal and bacillus Calmette-Guerin-induced urinary nitrate excretion over a 2-4 week time span.
 These experimental conditions should prove useful for further investigation on the role of macrophage NOM in host defense against intracellular microorganisms.
