Wang Y, Coceani F
Research Institute, Hospital for Sick Children, Toronto, Ontario, Canada.
Am J Physiol. 1994 Mar;266(3 Pt 2):H936-43. doi: 10.1152/ajpheart.1994.266.3.H936.
Endothelium-derived relaxing factor-nitric oxide (EDRF-NO) has been studied in isolated, pulmonary resistance vessels from term fetal lambs at a fetal (21 +/- 0.2 mmHg) and neonatal (69 +/- 0.4 mmHg) PO2. Bradykinin dose dependently (0.1-100 nM) relaxed arteries and veins that had been precontracted with a thromboxane A2 analogue. Their response did not differ at low PO2, whereas the response of the arteries was greater at high PO2. Sodium nitroprusside was almost as potent as bradykinin on the arteries, but its action did not vary with PO2. Acetylcholine also relaxed the arteries at higher concentrations (0.1-100 microM). N omega-mono-methyl-L-arginine (L-NMMA) and N omega-nitro-L-arginine methyl ester (L-NAME) (both at 100 microM) weakly contracted arteries at low PO2. The contraction to L-NAME, but not L-NMMA, increased with the PO2. In the arteries, L-NAME had no effect on bradykinin relaxation at low PO2, whereas it was an inhibitor at high PO2. Conversely, L-NMMA slightly inhibited bradykinin relaxation regardless of PO2. In the veins, L-NAME transiently increased basal tone and inhibited bradykinin relaxation at either PO2. Indomethacin (2.8 microM) had no effect on arteries at low PO2, whereas it was a constrictor at high PO2. No indomethacin constriction occurred in the veins. We conclude that fetal pulmonary resistance vessels possess an EDRF-NO relaxing mechanism that is stimulated by bradykinin. In the arteries, this mechanism is more effective at high PO2.(ABSTRACT TRUNCATED AT 250 WORDS)
内皮源性舒张因子-一氧化氮（EDRF-NO）已在足月胎羊离体肺阻力血管中进行了研究，研究时的胎儿血氧分压（PO2）为（21±0.2 mmHg），新生儿血氧分压为（69±0.4 mmHg）。缓激肽剂量依赖性地（0.1 - 100 nM）舒张已用血栓素A2类似物预收缩的动脉和静脉。在低血氧分压时，它们的反应无差异，而在高血氧分压时，动脉的反应更强。硝普钠对动脉的作用几乎与缓激肽一样有效，但它的作用不随血氧分压而变化。乙酰胆碱在较高浓度（0.1 - 100 μM）时也能舒张动脉。Nω-单甲基-L-精氨酸（L-NMMA）和Nω-硝基-L-精氨酸甲酯（L-NAME）（均为100 μM）在低血氧分压时使动脉轻度收缩。对L-NAME而非L-NMMA的收缩作用随血氧分压升高而增强。在动脉中，L-NAME在低血氧分压时对缓激肽舒张无影响，而在高血氧分压时是一种抑制剂。相反，L-NMMA无论血氧分压如何都能轻微抑制缓激肽舒张。在静脉中，L-NAME短暂增加基础张力并在任一血氧分压时抑制缓激肽舒张。吲哚美辛（2.8 μM）在低血氧分压时对动脉无影响，而在高血氧分压时是一种收缩剂。静脉中未出现吲哚美辛引起的收缩。我们得出结论，胎儿肺阻力血管具有由缓激肽刺激的EDRF-NO舒张机制。在动脉中，该机制在高血氧分压时更有效。（摘要截短至250字）
