Theis J G, Toyoda O, Coceani F
Research Institute, Hospital for Sick Children, Toronto, ON, Canada.
Can J Physiol Pharmacol. 1998 Feb;76(2):182-7.
We have recently shown that isolated pulmonary resistance arteries of the fetal lamb have prostaglandin (PG) I2 based and nitric oxide (NO) based relaxing mechanisms, which are activated by oxygen (at neonatal levels) and bradykinin. The present study was carried out to ascertain whether these mechanisms remain operational after removal of the endothelium. Endothelium-denuded vessels pre-equilibrated at a neonatal Po2 were not affected by indomethacin (2.8 microM), while they contracted weakly to NG-nitro-L-arginine methyl ester (L-NAME, 100 microM). However, the latter response did not reach significance and resembled that of intact vessels at fetal Po2. Bradykinin (0.1-100 nM) dose dependently (from 1-3 nM upwards) relaxed endothelium-denuded arteries that had been precontracted with a thromboxane (TX) A2 analog (ONO-11113, 0.1 microM) or excess potassium (5 mM Ca2+ in K(+)-Krebs) at a neonatal Po2. The response was the same under the two conditions, but it was smaller than that of intact arteries. Bradykinin relaxation of ONO-11113-contracted arteries was completely or nearly completely inhibited by indomethacin and L-NAME. We conclude that endothelium-denuded, pulmonary resistance arteries maintain PG (conceivably PGI2) mediated and NO-mediated relaxing mechanisms. These extra-endothelial mechanisms are activated by bradykinin but not by oxygen.
我们最近发现，胎羊的离体肺阻力动脉具有基于前列腺素（PG）I2和一氧化氮（NO）的舒张机制，这些机制可被氧气（新生儿水平）和缓激肽激活。本研究旨在确定去除内皮后这些机制是否仍然有效。在新生儿氧分压下预平衡的去内皮血管不受吲哚美辛（2.8微摩尔）影响，而对NG-硝基-L-精氨酸甲酯（L-NAME，100微摩尔）有微弱收缩。然而，后者的反应未达到显著水平，且与胎儿氧分压下完整血管的反应相似。在新生儿氧分压下，缓激肽（0.1 - 100纳摩尔）剂量依赖性地（从1 - 3纳摩尔以上）使已用血栓素（TX）A2类似物（ONO - 11113，0.1微摩尔）或过量钾（在含钾的 Krebs 液中5毫摩尔钙离子）预收缩的去内皮动脉舒张。在两种情况下反应相同，但比完整动脉的反应小。吲哚美辛和L-NAME完全或几乎完全抑制了缓激肽对ONO - 11113收缩动脉的舒张作用。我们得出结论，去内皮的肺阻力动脉维持PG（可能是PGI2）介导和NO介导的舒张机制。这些内皮外机制可被缓激肽激活，但不能被氧气激活。
