Forslund T, Tikkanen I, Fyhrquist F
Acta Pharmacol Toxicol (Copenh). 1983 Jul;53(1):78-80. doi: 10.1111/j.1600-0773.1983.tb01871.x.
Serum ACE activity increased as expected about three-fold following six weeks of captopril (30 mg/kg/day) treatment in Wistar rats (n = 9). The effect on serum and lung ACE activity and concentration, respectively, was studied after captopril discontinuation. Serum ACE activity was measured at start and 3, 6, and 12 days after captopril withdrawal. The approximal half-life of serum ACE activity was 72 hours as judged from the decrease rate after stimulated ACE biosynthesis induced by captopril. No differences in lung plasma membranes and lung homogenate ACE concentrations between treated and untreated rats were observed 12 days after discontinuation of captopril treatment. Serum ACE activity remained unchanged in the control rats (n = 9). We conclude that induction of ACE biosynthesis in the rat is reversible after withdrawal of captopril.
在Wistar大鼠(n = 9)中,卡托普利(30毫克/千克/天)治疗六周后,血清血管紧张素转换酶(ACE)活性如预期增加了约三倍。在停用卡托普利后,分别研究了其对血清和肺ACE活性及浓度的影响。在停用卡托普利时及停药后3天、6天和12天测量血清ACE活性。根据卡托普利诱导ACE生物合成后其下降速率判断,血清ACE活性的近似半衰期为72小时。在停用卡托普利治疗12天后,未观察到治疗组和未治疗组大鼠肺细胞膜和肺匀浆中ACE浓度的差异。对照大鼠(n = 9)的血清ACE活性保持不变。我们得出结论,停用卡托普利后,大鼠体内ACE生物合成的诱导是可逆的。