Mullane K M, Moncada S
Eur J Pharmacol. 1980 Sep 5;66(4):355-65. doi: 10.1016/0014-2999(80)90468-9.
The effect of angiotensin-converting enzyme inhibition by captopril on the release of a prostacyclin-like substance by bradykinin, angiotensin I and angiotensin II was studied by means of the blood-bathed bioassay technique of Vane. Administration of captopril abolished the release of prostacyclin-like substance induced by angiotensin I, potentiated the release provoked by bradykinin and did not alter that due to angiotensin II. Potentiation of the bradykinin-induced renal vasodilatation with captopril could be completely reversed by indomethacin, which also abolished the kinin-induced release of prostacyclin-like substance. Potentiation of the bradykinin-induced hypotension was markedly attenuated but not completely reversed by cyclo-oxygenase inhibition. It is suggested that following converting inhibition increased production of prostacyclin by elevated kinin levels may contribute to the antihypertensive action of angiotensin-converting enzyme inhibitors.
采用Vane的血浴生物测定技术，研究了卡托普利抑制血管紧张素转换酶对缓激肽、血管紧张素I和血管紧张素II释放类前列环素物质的影响。给予卡托普利可消除血管紧张素I诱导的类前列环素物质的释放，增强缓激肽引起的释放，而对血管紧张素II引起的释放无影响。吲哚美辛可完全逆转卡托普利增强的缓激肽诱导的肾血管舒张，吲哚美辛还可消除缓激肽诱导的类前列环素物质的释放。环氧化酶抑制可使缓激肽诱导的低血压增强作用明显减弱，但不能完全逆转。提示在转换酶抑制后，缓激肽水平升高导致类前列环素生成增加，可能有助于血管紧张素转换酶抑制剂的降压作用。
