The interactions between L-arginine, the source of nitric oxide formation, and NG-nitro-L-arginine (L-NOARG), an inhibitor of nitric oxide synthase were examined in isolated rat aorta. Carbachol induced endothelium-dependent relaxation was used to study the constitutive form of the enzyme, whereas the loss of contraction tonicity to phenylephrine following incubation of endothelium free rings with interleukin 1 was used to investigate the smooth muscle inducible form. L-NOARG is a potent inhibitor of the two types of the enzyme in the rat aorta. However, the effects of L-NOARG on the constitutive (endothelial) vascular NO synthase were partially prevented, but not reversed, by L-arginine. In contrast, L-arginine fully reversed the action of L-NOARG on the smooth muscle inducible form of NO synthase. The selective reversibility of L-NOARG on the inducible, by comparison with the constitutive form of nitric oxide synthase present in the vasculature, may represent a limitation in the use of this type of compounds in the treatment of the systemic arterial hypotension observed during septic shock.