Hui S C, Dai S, Ogle C W
Clin Exp Pharmacol Physiol. 1984 Nov-Dec;11(6):621-5. doi: 10.1111/j.1440-1681.1984.tb00875.x.
In chloralose anaesthetized rats, intravenous administration of captopril, SQ 20881, SA 446 or MK 421 (0.5 mg/kg) potentiated the depressor responses to arachidonic acid 3 mg/kg given intravenously. Same doses of the above angiotensin converting enzyme inhibitors caused an approximately 100-fold decrease in sensitivity to the pressor effects of angiotensin I, with a concomitant similar increase in sensitivity to the depressor effects of bradykinin. Depressor responses to arachidonic acid, both before and after administering the converting enzyme inhibitors, were abolished by intravenous indomethacin (5 mg/kg). These results suggest that increased synthesis of prostaglandins in the circulation may contribute to the hypotensive effect of the angiotensin converting enzyme inhibitors, a group of newly developed antihypertensive agents.
在水合氯醛麻醉的大鼠中,静脉注射卡托普利、SQ 20881、SA 446或MK 421(0.5毫克/千克)可增强静脉注射3毫克/千克花生四烯酸后的降压反应。相同剂量的上述血管紧张素转换酶抑制剂使对血管紧张素I升压作用的敏感性降低约100倍,同时对缓激肽降压作用的敏感性有类似程度的增加。静脉注射吲哚美辛(5毫克/千克)可消除在给予转换酶抑制剂前后对花生四烯酸的降压反应。这些结果表明,循环中前列腺素合成增加可能有助于血管紧张素转换酶抑制剂(一类新开发的抗高血压药物)的降压作用。