Abstract:
Studiesin vivo in fetal sheep have shown that bradykininis released following oxygenation of the lungs and is at least partlyresponsible for normal pulmonary vasodilatation in the transition from fetalto extrauterine life. Part of this action involves secondary release ofprostaglandin I<emph type="8">2 (PGI<emph type="8">2). Invarious adult vessels, bradykinin also stimulates the release of a powerfulendothelium-derived relaxing factor (EDRF).Studiesin vitro were designed (using a modification ofthe bioassay cascade superfusion technique) to determine whethernon-PGI<emph type="8">2-related perinatal pulmonary vasodilatation ismediated by an EDRF. Superfused, precontracted, endothelium-denuded strips offetal sheep thoracic aorta and the maternal sheep main pulmonary artery servedas detectors of an EDRF released from isolated, perfused fetal sheep pulmonaryarteries. Bradykinin, in the presence of indomethacin to block PGI2 synthesis,caused perfused fetal pulmonary arteries to release an EDRF, which generated adose-dependent relaxation (24% for 1·0µM,16·8% for 0·1 µM, and 10% for0·01 µM bradykinin). Thus, bradykinin can produce perinatalpulmonary vasodilatation via a mechanism involving the endothelium-dependentsynthesis of an EDRF.