Angiotensin-Converting Enzyme Inhibitors

作者：Izzo Joseph L Jr^*; Weir Matthew R

来源：Journal of Clinical Hypertension, 2011, 13(9): 667-675.

DOI：10.1111/j.1751-7176.2011.00508.x

Key Points and Recommendations
In addition to hypertension, angiotensin-converting enzyme inhibitors are indicated for treatment of patients at high risk for coronary artery disease, after myocardial infarction, with dilated cardiomypathy, or with chronic kidney disease.
The most familiar angiotensin-converting enzyme subtype, angiotensin-converting enzyme-1 (kininase II), cleaves the vasoconstrictor octapeptide angiotensin II from its inactive decapeptide precursor, angiotensin I, while simultaneously inactivating the vasodilator bradykinin.
Biochemical pathways within and around the renin-angiotensin system are highly species-specific; there is little evidence that "angiotensin-converting enzyme bypass pathways" have major clinical implications in humans.
Dietary sodium loading can diminish or abolish the antihypertensive effect of an angiotensin-converting enzyme inhibitor, while salt restriction or concomitant diuretic therapy enhances it.
Dose-response curves with angiotensin-converting enzyme inhibitors are quite flat but their peak effects vary in different individuals.
Increased serum creatinine (decreased glomerular filtration rate) during acute or chronic angiotensin-converting enzyme inhibition identifies individuals likely to experience long-term renal protective benefits.
Angiotensin-converting enzyme inhibitors are contraindicated in pregnancy due to fetal toxicity.
Use of angiotensin-converting enzymes can be limited by idiosyncratic reactions (cough or angioedema), hyperkalemia (usually in cardiac or renal failure or with combined renin-angiotensin blockade) or hypotension (usually with severe volume-depletion or cardiac failure). J Clin Hypertens (Greenwich). 2011; 13: 667-675.

• 出版日期2011-9