Angiotensin-converting enzyme inhibition and salt in experimental myocardial infarction

被引:12
|
作者
Yoshida, K [1 ]
Kohzuki, M
Casley, DJ
Johnston, CI
机构
[1] Tohoku Univ, Grad Sch Med, Sect Internal Med & Disabil Prevent, Sendai, Miyagi 9808574, Japan
[2] Univ Melbourne, Austin & Repatriat Med Ctr, Dept Med, Heidelberg, Vic, Australia
关键词
angiotensin; converting enzyme inhibitor; myocardial infarction; cardiac hypertrophy; sodium; rats;
D O I
10.1097/00005344-199809000-00004
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
It is well known that angiotensin-converting enzyme inhibitors attenuate progressive ventricular enlargement or hypertrophy after myocardial infarction and that cardiac angiotensin-converting enzyme activity is increased in the rat model of myocardial infarction. Tn this study, to determine whether the beneficial effects of angiotensin-converting enzyme inhibition on cardiac hypertrophy after myocardial infarction are due to a reduction in ventricular afterload or to inhibition of cardiac angiotensin-converting enzyme, we used sodium loading during angiotensin-converting enzyme inhibition. The rat model of myocardial infarction was treated with a vehicle, 1% saline, as drinking fluid, perindopril (2 mg/kg/day), or 1% saline as drinking fluid plus perindopril (2 mg/kg/day) for 6 weeks. Perindopril reduced blood pressure, prevented cardiac hypertrophy, and inhibited cardiac angiotensin-converting enzyme. The effects of perindopril on blood pressure and cardiac hypertrophy were abolished by sodium loading, which did not alter the degree of cardiac angiotensin-converting enzyme inhibition. Thus the actions of perindopril on cardiac hypertrophy depend more on blood pressure reduction than on cardiac angiotensin-converting enzyme inhibition in the rat model of myocardial infarction.
引用
收藏
页码:357 / 365
页数:9
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