N-G-NITRO-L-ARGININE CONTRACTS VASCULAR SMOOTH-MUSCLE BY AN ENDOTHELIUM-INDEPENDENT MECHANISM

We characterized the contractile effect of the nitric oxide (NO) synth ase inhibitor N-G-nitro-L-arginine (L-NNA) in endothelium-denuded rat aortic rings. Incubation with L-NNA (4 x 10(-6)-6.4 x 10(-5)M) for 5 h dose-dependently contracted endothelium-denuded aortic rings. In cont rast, incubation with N-G-nitro-D-arginine (D-NNA 6 x 10(-6)-4 x 10(-4 )M), diphenyleneiodonium (DPI, NO synthase inhibitor, 3.2 x 10(-6)M) o r dexamethasone (10(-7)M, inhibitor of expression of inducible NO synt hase) did not contract the denuded rings. The L-NNA-induced contractio n was not significantly altered by the presence of the endothelium or by pretreatment with L-arginine (L-Arg 2 x 10(-3)M) or lipopolysacchar ide (100 ng/ml). These results suggest that L-NNA causes slow contract ion of endothelium-denuded vascular smooth muscle (VSM) by a mechanism independent of the inhibition of constitutive or inducible NO biosynt hesis.