Key result
L-NNA induces dose-dependent vascular smooth muscle contraction through a mechanism independent of NO inhibition.
Why the study?
The contractile effect of the nitric oxide synthase inhibitor NG-nitro-L-arginine (L-NNA) on vascular smooth muscle independent of endothelium was not characterized.
L-NNA causes slow contraction of endothelium-denuded vascular smooth muscle by a mechanism independent of the inhibition of constitutive or inducible NO biosynthesis.
Findings in isolated vessels warrant caution before clinical extrapolation; leaves open mechanisms of NO synthase inhibition in vascular tissue.
We characterized the contractile effect of the nitric oxide (NO) synthase inhibitor NG-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 contrast, incubation with NG-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) or dexamethasone (10(-7) M, inhibitor of expression of inducible NO synthase) did not contract the denuded rings. The L-NNA-induced contraction was not significantly altered by the presence of the endothelium or by pretreatment with L-arginine (L-Arg 2 x 10(-3) M) or lipopolysaccharide (100 ng/ml). These results suggest that L-NNA causes slow contraction of endothelium-denuded vascular smooth muscle (VSM) by a mechanism independent of the inhibition of constitutive or inducible NO biosynthesis.
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Wang et al. (1994) studied this question. NG-nitro-L-arginine (L-NNA) vs. NG-nitro-D-arginine (D-NNA), diphenyleneiodonium (DPI), or dexamethasone was evaluated on Contractile effect. L-NNA caused slow, dose-dependent contraction of endothelium-denuded vascular smooth muscle by a mechanism independent of NO biosynthesis inhibition.
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