In guinea-pig isolated lungs perfused with Krebs solution, captopril (10 microM) inhibited the metabolism of bradykinin (Bk) and the conversion of angiotensin I to angiotensin II, as measured by bioassay. Captopril significantly enhanced Bk-stimulated output of prostacyclin. 2. In bovine aortic endothelial cells grown on microcarrier beads, captopril (10 microM) did not affect the release of prostacyclin or of endothelium-derived relaxing factor (EDRF) induced by Bk. 3. Angiotensin I or angiotensin II did not release prostacyclin from guinea-pig isolated lungs or bovine aortic endothelial cells. They were also ineffective as releasers of EDRF from bovine aortic endothelial cells. 4. Thus, activation of angiotensin converting enzyme is not involved in the release of prostacyclin from guinea-pig isolated lungs or bovine aortic endothelial cells, or in release of EDRF from bovine aortic endothelial cells.
摘要
在用 Krebs 溶液灌注的豚鼠离体肺中,通过生物测定法测量,卡托普利(10微摩尔)抑制缓激肽(Bk)的代谢以及血管紧张素 I 向血管紧张素 II 的转化。卡托普利显著增强了 Bk 刺激的前列环素输出。2. 在微载体珠上生长的牛主动脉内皮细胞中,卡托普利(10微摩尔)不影响 Bk 诱导的前列环素或内皮衍生舒张因子(EDRF)的释放。3. 血管紧张素 I 或血管紧张素 II 不会从豚鼠离体肺或牛主动脉内皮细胞中释放前列环素。它们作为从牛主动脉内皮细胞释放 EDRF 的物质也无效。4. 因此,血管紧张素转换酶的激活不参与豚鼠离体肺或牛主动脉内皮细胞中前列环素的释放,也不参与牛主动脉内皮细胞中 EDRF 的释放。