Di Nicolantonio R, Hutchinson J S, Takata Y, Veroni M
Br J Pharmacol. 1983 Nov;80(3):405-8. doi: 10.1111/j.1476-5381.1983.tb10709.x.
The transient vasodepressor action of Met-enkephalin (10-80 micrograms kg-1, i.v.) in anaesthetized rats was significantly potentiated by the angiotensin-converting enzyme inhibitor, captopril (2 mg kg-1, i.v.); at this dose, it failed to modify the transient vasodepressor action of the non-specific vasodilator, nitroprusside (2.5, 5.0, 10 micrograms kg-1, i.v.). Captopril (2 mg kg-1, i.v.) caused a slow, progressive fall in the blood pressure of anaesthetized spontaneously hypertensive (SH) rats when compared to vehicle-treated controls. Pretreatment with naloxone (1.5 mg kg-1, i.v.) 30 min earlier failed to alter significantly the hypotensive action of captopril in anaesthetized SH rats. It was concluded that although captopril potentiated the vasodepressor action of Met-enkephalin in anaesthetized normotensive rats, potentiation of endogenous opioids does not appear to be involved in the hypotensive action of captopril in anaesthetized SH rats.
在麻醉大鼠中,甲硫氨酸脑啡肽(10 - 80微克/千克,静脉注射)的短暂血管降压作用被血管紧张素转换酶抑制剂卡托普利(2毫克/千克,静脉注射)显著增强;在此剂量下,它未能改变非特异性血管扩张剂硝普钠(2.5、5.0、10微克/千克,静脉注射)的短暂血管降压作用。与给予赋形剂的对照组相比,卡托普利(2毫克/千克,静脉注射)使麻醉的自发性高血压(SH)大鼠的血压缓慢、逐渐下降。提前30分钟用纳洛酮(1.5毫克/千克,静脉注射)预处理,未能显著改变卡托普利对麻醉的SH大鼠的降压作用。得出的结论是,虽然卡托普利增强了甲硫氨酸脑啡肽在麻醉的正常血压大鼠中的血管降压作用,但内源性阿片类物质的增强似乎不参与卡托普利在麻醉的SH大鼠中的降压作用。