Thorin-Trescases N, Hamilton C A, Reid J L, McPherson K L, Jardine E, Berg G, Bohr D, Dominiczak A F
University Department of Medicine and Therapeutics, Gardiner Institute, Department of Cardiac Surgery, Western Infirmary, Glasgow, United Kingdom.
Am J Physiol. 1995 Mar;268(3 Pt 2):H1122-32. doi: 10.1152/ajpheart.1995.268.3.H1122.
To characterize the L-arginine/nitric oxide (NO) pathway in human vascular smooth muscle (VSM), contractile responses of isolated internal mammary arteries (IMA) and saphenous veins (SV) were observed after induction of NO synthase by interleukin-1 beta (IL-1 beta) or by lipopolysaccharide (LPS). In IL-1 beta-treated endothelium-denuded rings, contractile responses to phenylephrine were reduced in SV rings only. Maximum phenylephrine-induced contraction was depressed by approximately 50%. This was not modified by the presence of indomethacin, NG-nitro-L-arginine methyl ester (L-NAME), or methylene blue (MeB). In LPS-treated vessels, contractile responses were depressed in both SV and IMA rings (40%), and this was not affected by indomethacin. In SV, L-NAME, NG-monomethyl-L-arginine, or MeB did not affect the inhibitory effect of LPS, whereas the effect was reversed in IMA by these inhibitors. In LPS-treated IMA, but not in SV, exogenous L-arginine evoked significant vasodilation (20%). We conclude that VSM of the human IMA possesses an L-arginine/NO pathway inducible by LPS. In SV, LPS or IL-1 beta treatment inhibits contraction by an unidentified system that is not dependent on NO synthase or on guanylate cyclase activities.
为了表征人血管平滑肌（VSM）中的L-精氨酸/一氧化氮（NO）途径，在用白细胞介素-1β（IL-1β）或脂多糖（LPS）诱导一氧化氮合酶后，观察了离体乳内动脉（IMA）和大隐静脉（SV）的收缩反应。在经IL-1β处理的去内皮环中，仅SV环对去氧肾上腺素的收缩反应降低。去氧肾上腺素诱导的最大收缩降低了约50%。吲哚美辛、NG-硝基-L-精氨酸甲酯（L-NAME）或亚甲蓝（MeB）的存在并未改变这种情况。在经LPS处理的血管中，SV和IMA环的收缩反应均降低（40%），且这不受吲哚美辛影响。在SV中，L-NAME、NG-单甲基-L-精氨酸或MeB不影响LPS的抑制作用，而在IMA中这些抑制剂可逆转该作用。在经LPS处理的IMA中，而非SV中，外源性L-精氨酸可引起显著的血管舒张（20%）。我们得出结论，人IMA的VSM具有可被LPS诱导的L-精氨酸/NO途径。在SV中，LPS或IL-1β处理通过一种不依赖于一氧化氮合酶或鸟苷酸环化酶活性的未知系统抑制收缩。
