Isolated pulmonary resistance arteries from term fetal lambs have nitric oxide (NO)- and prostaglandin-mediated relaxing mechanisms which are activated when PO2 is raised from fetal to neonatal levels. The same vessels contract under hypoxia, and the contraction has been ascribed to endothelin-1 (ET-1). We have now studied these vasoeffector mechanisms before term (0.7 and 0.65 gestation) with the objective of determining whether their activity correlates with the development of susceptibility to oxygen changes. Experiments were carried out at neonatal PO2, when expectedly relaxing mechanisms are maximally expressed, or under hypoxia. At either fetal age, the NO synthesis inhibitor, NG-nitro-L-arginine methyl ester (100 μM), had no effect on basal tone, while indomethacin (2.8 μM) was a weak constrictor. Premature arteries did not contract when first exposed to hypoxia, but they responded marginally to a second exposure. The same arteries contracted strongly to a thromboxane A2 analogue (ONO-11113, 0.1 μM) and ET-1 (10 nM), while their contraction to activating solution (5 mM Ca2+ in K+-Krebs solution) was small and variable. At 0.7 gestation, bradykinin (0.1–100 nM), acetylcholine (0.01–10 μM), and sodium nitroprusside (0.1 nM to 10 μM) dose-dependently relaxed arteries precontracted with ONO-11113. Conversely, at 0.65 gestation the relaxation to bradykinin and acetylcholine was not dose-dependent and tended to be weaker. We conclude that preterm pulmonary arteries have viable effector mechanisms for contraction and relaxation. However, the capability for these mechanisms to be activated by PO2 changes is markedly curtailed.

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