用血管紧张素转换酶抑制化合物MK-421诱导大鼠肺中的血管紧张素转换酶。

Induction of angiotensin-converting enzyme with the ACE inhibitory compound MK-421 in rat lung.

作者信息

Forslund T, Fyhrquist F, Grönhagen-Riska C, Tikkanen I

出版信息

Eur J Pharmacol. 1982 May 7;80(1):121-5. doi: 10.1016/0014-2999(82)90186-8.

Abstract

Having observed that treatment of rats with captopril led to an increased ACE activity in serum and ACE concentration in lungs, we treated female Wistar Kyoto rats for 7 days with the esterified ACE inhibitor, MK-421 (1.0 mg/kg body weight per day), administered by Alzet osmotic minipump. Serum ACE activity decreased by 67% during MK-421 treatment when measured in non-dialyzed serum samples. Removal of the drug by dialysis unmasked a 280% increase of serum ACE activity. ACE concentration of crude lung homogenate increased 134% in MK-421-treated rats and ACE concentration in purified pulmonary plasma membranes increased by 34%. The increase of serum and lung ACE in MK-421-treated rats was similar to that seen in rats treated with captopril, and was probably due to induction of ACE biosynthesis. The mechanisms of this induction are unknown.

摘要

观察到用卡托普利治疗大鼠会导致血清中ACE活性增加以及肺中ACE浓度升高后，我们用Alzet渗透微型泵给雌性Wistar Kyoto大鼠连续7天注射酯化ACE抑制剂MK - 421（每天1.0毫克/千克体重）。在未透析的血清样本中测量时，MK - 421治疗期间血清ACE活性降低了67%。通过透析去除药物后，血清ACE活性增加了280%。MK - 421治疗的大鼠粗肺匀浆中ACE浓度增加了134%，纯化的肺质膜中ACE浓度增加了34%。MK - 421治疗的大鼠血清和肺中ACE的增加与用卡托普利治疗的大鼠相似，可能是由于ACE生物合成的诱导。这种诱导的机制尚不清楚。