Fyhrquist F, Grönhagen-Riska C, Forslund T, Tikkanen I
Am J Cardiol. 1982 Apr 21;49(6):1508-10. doi: 10.1016/0002-9149(82)90370-8.
In spontaneously hypertensive rats, treatment with captopril, 0.2 g/liter of drinking fluid for 12 to 24 weeks, caused a threefold increase in serum angiotensin I-converting enzyme activity. Angiotensin I-converting enzyme increased 25 to 120 percent in lung plasma membranes. The elution profile of angiotensin I-converting enzyme on DEAE cellulose and after gel filtration on Sepharose 4B was unchanged by captopril. The Km value value also remained unchanged. In Wistar rats subjected to bilateral adrenalectomy, treatment with the same dose of captopril for 3 days resulted in increased serum angiotensin I-converting enzyme activity in both sham-operated and adrenalectomized rats, but angiotensin I-converting enzyme concentration increased in lung plasma membranes from sham-operated rats and captopril-treated rats only. We conclude that captopril causes induction of angiotensin-converting enzyme biosynthesis in spontaneously hypertensive and Wistar rats. The change is a quantitative one. Intact adrenal glands may be important for the incorporation of angiotensin I-converting enzyme into lung membranes.
在自发性高血压大鼠中,用卡托普利(每升饮水中含0.2克,持续12至24周)治疗后,血清血管紧张素I转换酶活性增加了两倍。肺细胞膜中的血管紧张素I转换酶增加了25%至120%。卡托普利未改变血管紧张素I转换酶在DEAE纤维素上的洗脱图谱以及在Sepharose 4B上凝胶过滤后的洗脱图谱。米氏常数(Km值)也保持不变。在接受双侧肾上腺切除术的Wistar大鼠中,用相同剂量的卡托普利治疗3天,导致假手术组和肾上腺切除组大鼠的血清血管紧张素I转换酶活性均增加,但仅假手术组和卡托普利治疗组大鼠肺细胞膜中的血管紧张素I转换酶浓度增加。我们得出结论,卡托普利可导致自发性高血压大鼠和Wistar大鼠中血管紧张素转换酶生物合成的诱导。这种变化是定量的。完整的肾上腺对于血管紧张素I转换酶掺入肺膜可能很重要。