L-arginine availability is not limiting for nitric oxide generation from recombinant endothelial nitric oxide synthase

L-Arginine (L-Arg) may be limiting for inducible nitric oxide synthase (NOS ) activity and under certain circumstances, such as increased concentration s of a NOS inhibitor, may also be limiting for endothelial NOS activity. It is unknown if L-Arg is limiting for recombinant eNOS activity in the vascu lar wall after adenoviral mediated gene transfer. Our aim was to examine, i f L-Arg is limiting for recombinant eNOS activity in the normal or atherosc lerotic vessel wall. Rings of rabbit aorta from chow or cholesterol fed ani mals were transduced with adenovirus vector encoding eNOS (AdeNOS) or beta- galactosidase (Ad beta Gal). After 24 h, transgene expression was confirmed and vasomotor studies were performed in the absence or presence of L-Arg. During maximal contractions to phenylephrine (10(-5) M), L-Arg (3 mM) was a dded to the organ chamber for 30 min. Subsequently, relaxations to acetylch oline during half-maximal contractions were obtained. In the chow- and chol esterol-fed animals, relaxations were significantly enhanced in the NOS and NOS + L-Arg groups compared to the beta Gal and beta Gal + L-Arg groups. T here was no difference between NOS and NOS + L-Arg or beta Gal and beta Gal + L-Arg rings from chow- or cholesterol-fed animals. While gene transfer o f eNOS enhances endothelium-dependent vasorelaxation in the normal and athe rosclerotic vessel wall, L-arginine is not limiting for recombinant eNOS ac tivity. Copyright(C)1999 S. Karger AG, Basel.