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PubMed · 7602784

[Angiotensin-I converting enzyme].

Abstract

Angiotensin I-converting enzyme (ACE) converts the largely inactive decapeptide angiotensin I to the active octapeptide angiotensin II. ACE is a key component of the renin-angiotensin system that has long been suspected to play a role in the pathogenesis of hypertension and cardiovascular disease. The ACE gene spans 21 kilobases and consists of 26 exons, and two different mRNAs and endothelial and testicular ACE are transcribed from the ACE gene. Circulating ACE probably originates from proteolytic cleavage of the hydrophobic anchor and passive leakage of the membrane-bound enzyme. Normal serum ACE by spectrophotometric assay is very low (8.3-21.4 microliters/ml). The abnormally elevated ACE levels is indeed a diagnostic aid in sarcoidosis. The ACE gene has 287 base pair insertion/deletion polymorphism in intron 16. The ACE deletion polymorphism appears to be associated with increased risk for myocardial infarction in the Caucasian and Japanese population. Recently in multicenter clinical trials (SAVE), administration of inhibitors of ACE were shown to decrease cardiac events after myocardial infarction.

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BibTeXRIS

K Nakai, T Syoh, K Hiramori. 1995. [Angiotensin-I converting enzyme].. https://pubmed.ncbi.nlm.nih.gov/7602784/

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Angiotensin-Converting Enzyme Inhibitors↗

Renin-induced hypertension in Wilms tumor patients.

BACKGROUND: Since the report that hypertension associated with Wilms tumor (WT) may be renin-induced, no larger series than 13 patients have been published. Nevertheless, angiotensin converting enzyme (ACE) inhibitors have become treatment of choice for hypertension in WT patients. The purpose of this study was to investigate the correlation between plasma renin levels and blood pressure in a larger cohort of WT patients. PROCEDURE: In this retrospective, single-center study, data on blood pressure and plasma renin were analyzed in 86 WT patients treated according to the consecutive SIOP protocols 6, 9, 93-01, and 2001. RESULTS: At diagnosis, 47 WT patients suffered from hypertension (55%). In 31 of these patients plasma renin levels were analyzed; increased plasma renin levels were found in 25/31 patients (81%). In contrast, normal plasma renin levels were measured in 8/13 of the patients with a normal blood pressure (P = 0.012). Twenty-eight children received antihypertensive treatment before surgery, in 25 of them blood pressure normalized before surgery. Blood pressure was normal directly after surgery in all patients but 4, in whom blood pressure recovered to normal within a few weeks. CONCLUSIONS: This retrospective study shows that hypertension in WT patients is associated with elevated plasma renin levels, indicating that ACE inhibitors may be a good therapeutic option in at least a subset of WT patients with hypertension before nephrectomy.

Angiotensin-Converting Enzyme Inhibitors↗