Wang Y X, Pang C C
Department of Pharmacology & Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, Canada.
J Cardiovasc Pharmacol. 1994 Jul;24(1):59-63. doi: 10.1097/00005344-199407000-00011.
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.
我们研究了一氧化氮（NO）合酶抑制剂NG-硝基-L-精氨酸（L-NNA）对去内皮大鼠主动脉环的收缩作用。用L-NNA（4×10⁻⁶ - 6.4×10⁻⁵ M）孵育5小时，去内皮主动脉环呈剂量依赖性收缩。相比之下，用NG-硝基-D-精氨酸（D-NNA 6×10⁻⁶ - 4×10⁻⁴ M）、二苯乙烯碘鎓（DPI，NO合酶抑制剂，3.2×10⁻⁶ M）或地塞米松（10⁻⁷ M，诱导型NO合酶表达抑制剂）孵育，并未使去内皮环收缩。内皮的存在、用L-精氨酸（L-Arg 2×10⁻³ M）或脂多糖（100 ng/ml）预处理，均未显著改变L-NNA诱导的收缩。这些结果表明，L-NNA通过一种独立于抑制组成型或诱导型NO生物合成的机制，引起去内皮血管平滑肌（VSM）的缓慢收缩。
