Fantone J C, Schrier D, Weingarten B
J Clin Invest. 1982 Jun;69(6):1207-11. doi: 10.1172/jci110559.
Systemic treatment of rats with captopril (50 mg/kg body wt per os), a specific competitive inhibitor of angiotensin l-converting enzyme, significantly inhibits vascular permeability changes induced by the intradermal injection of the vasoactive mediators histamine, bradykinin, serotonin, and compound 48/80. This effect of captopril is both dose- and time-dependent with approximately 60% inhibition of edema formation observed 7 h after captopril treatment (100 mg/kg body wt per os). The inhibitory effect of captopril on edema formation is temporally unrelated to the inhibition of serum angiotensin l-converting enzyme activity or serum prostaglandin E2 levels and is not inhibited by systemic treatment of rats with indomethacin. The data suggest that captopril may have potent antiinflammatory activity through as yet undefined mechanisms.
用卡托普利(每千克体重50毫克,口服)对大鼠进行全身治疗,卡托普利是血管紧张素I转换酶的特异性竞争性抑制剂,可显著抑制皮内注射血管活性介质组胺、缓激肽、血清素和化合物48/80所诱导的血管通透性变化。卡托普利的这种作用具有剂量和时间依赖性,在卡托普利治疗(每千克体重100毫克,口服)7小时后,观察到约60%的水肿形成受到抑制。卡托普利对水肿形成的抑制作用在时间上与血清血管紧张素I转换酶活性或血清前列腺素E2水平的抑制无关,并且不受用吲哚美辛对大鼠进行全身治疗的抑制。数据表明,卡托普利可能通过尚未明确的机制具有强大的抗炎活性。