ArticleInternational journal of hypertension2012
N-domain isoform of Angiotensin I converting enzyme as a marker of hypertension: populational study.
Article in International journal of hypertension, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Fecal ACE and ACE2 Activities Reflect Intestinal Shedding and Microbiota Modulation of Renin-Angiotensin System.Biology · 2026Article
- Is It Still Relevant to Discover New ACE Inhibitors from Natural Products? YES, but Only with Comprehensive Approaches to Address the Patients' Real Problems: Chronic Dry Cough and Angioedema.Molecules (Basel, Switzerland) · 2023Review
- Pediatric dyslipidemia is associated with increased urinary ACE activity, blood pressure values, and carotidal-femoral pulse wave velocity.Hypertension research : official journal of the Japanese Society of Hypertension · 2023Article
- Association of Ang-(1-7) and des-ArgHypertension research : official journal of the Japanese Society of Hypertension · 2021Article
- Characterization of angiotensin-converting enzyme 2 ectodomain shedding from mouse proximal tubular cells.PloS one · 2014Article
- Rosiglitazone treatment of type 2 diabetic db/db mice attenuates urinary albumin and angiotensin converting enzyme 2 excretion.PloS one · 2013Article
- Soluble urinary somatic angiotensin converting enzyme is overexpressed in patients with preeclampsia: a potential new marker for the disease?Hypertension in pregnancyArticle
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this paper was to investigate the presence of the urinary 90 kDa N-domain ACE in a cohort of the population from Vitoria, Brazil, to verify its association with essential hypertension since this isoform could be a possible genetic marker of hypertension. Anthropometric, clinical, and laboratory parameters of the individuals were evaluated (n = 1150) and the blood pressure (BP) was measured. The study population was divided according to ACE isoforms in urine as follows: ACE 65/90/190, presence of three ACE isoforms (n = 795), ACE 90(+) (65/90) (n = 186), and ACE 90(-) (65/190) (n = 169) based on the presence (+) or absence (-) of the 90 kDa ACE isoform. The anthropometric parameters, lipid profile, serum levels of uric acid, glucose, and the systolic and diastolic BP were significantly greater in the ACE 90(+) compared with the ACE 90(-) and ACE 65/90/190 individuals. We found that 98% of individuals from the ACE 90(+) group and 38% from the ACE 65/90/190 group had hypertension, compared to only 1% hypertensive individuals in the ACE 90(-) group. There is a high presence of the 90 kDa N-domain ACE isoform (85%) in the studied population. The percentile of normotensive subjects with three isoforms was 62%. Our findings could contribute to the development of new efficient strategy to prevent and treat hypertension to avoid the development of cardiovascular disease.
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Registered trials
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