Association of urinary 90 kDa angiotensin- converting enzyme with family history of hypertension and endothelial function in normotensive individuals

Teixeira, Anderson; Plavnik, Frida Liane; Fernandes, Fernanda Barrinha; Marson, O; Christofalo, Dejaldo Marcos de Jesus; Ajzen, Sérgio Aron; Sesso, Ricardo; Franco, Maria do Carmo Pinho; Casarini, Dulce Elena

doi:10.1590/s0100-879x2008005000017

Cited by 3 publications

(9 citation statements)

References 22 publications

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“…Profile of ACE isoforms in these three subjects are shown in Figure 1. The profile was obtained for urine of human subjects as described previously by our group [19, 25, 26]. …”

Section: Resultsmentioning

confidence: 99%

“…Recently we described the association of 90 kDa N-domain ACE with plasma inflammatory markers, endothelial function, and family history of hypertension. Our data suggested that the 90 kDa ACE may be a marker for hypertension [25, 26]. Therefore, the aim of this study was to investigate the presence of the urinary 90 kDa N-domain ACE in a large cohort of the general population and to determine its association with presence of hypertension and with associated factors that can contribute to development of high blood pressure.…”

Section: Introductionmentioning

confidence: 99%

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N-Domain Isoform of Angiotensin I Converting Enzyme as a Marker of Hypertension: Populational Study

Maluf-Meiken

Fernandes

Aragão

et al. 2012

International Journal of Hypertension

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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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“…Profile of ACE isoforms in these three subjects are shown in Figure 1. The profile was obtained for urine of human subjects as described previously by our group [19, 25, 26]. …”

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

N-Domain Isoform of Angiotensin I Converting Enzyme as a Marker of Hypertension: Populational Study

Maluf-Meiken

Fernandes

Aragão

et al. 2012

International Journal of Hypertension

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“…In order to confirm our hypothesis and based on the experimental methods used by Casarini et al [34,38], two urine collections should be made from pregnant women with PES, to analyze the presence and enzymatic activity of the 90 kDa ACE isoform: the first sample after 20 weeks gestation, and the second within 12 weeks after delivery.…”

Section: Urinary Detection Of the 90 Kda Ace Isoformmentioning

confidence: 88%

“…According to these studies, the 90 kDa ACE isoform may contribute to the early diagnosis of hypertension, assisting in the prevention of cardiovascular diseases [33][34][35][36][37][38].…”

Section: Kda Isoform -A Biomarker Of Hypertensionmentioning

confidence: 99%

“…The enzymatic activity of ACE isoforms is an additional analysis to confirm the presence of these proteins in urine, through their measurement using two substrates: Hippuryl-His-Leu (HHL) [39] to quantify the somatic ACE with 190 kDa and Z-Phe-His-Leu (ZPhe-HL) [43,44] to quantify the 90 and 65 kDa N-domains isoforms, as outlined in a technique by Casarini et al [34,38]. Determining the ZPhe-HL/HHL activity ratio indicates the highest quantity/activity of the N-domain isoform (90/65 kDa).…”

Section: Enzyme Activity Of the 90 Kda Isoformmentioning

confidence: 99%

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Angiotensin Converting Enzyme 90kDa isoform: Biomarker for diagnosis of preeclampsia?

et al. 2014

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Preeclampsia (PE), one of the leading gestational hypertensive diseases, is characterized by increased blood pressure (⩾140/90mmHg) and pathological proteinuria after 20weeks gestation. It is a complex, multifactorial syndrome with an unestablished etiology and cure. The search continues for a biomarker that could assist in the early prediction or diagnosis of PE, reducing the rate of maternal and fetal mortality. Based on the findings of Casarini et al. that suggest the 90kDa isoform of the Angiotensin Converting Enzyme (ACE) as a possible marker of hypertension, we hypothesized that this isoform may be present in pregnant women with PE, since they present a transient and spontaneous model of systemic arterial hypertension in pregnancy. We believe, therefore, that pregnant women with pure PE (PPE) express the ACE 90kDa isoform in urine, as well as having elevated isoform enzymatic activity, during pregnancy only. Postpartum, with the normalization of blood pressure, the protein isoform would no longer be expressed. Pregnant women with superimposed preeclampsia (SPE) would present the ACE 90kDa isoform both during and after the gestation period, and its enzymatic activity would remain high as they are chronically hypertensive. It is expected that normotensive pregnant women do not present this isoform in their urine as elevated blood pressure levels do not occur. Both normotensive and PPE affected pregnant women with a family history of hypertension, will possibly express the ACE 90kDa isoform before pregnancy and may become hypertensive, only after some years, through the influence of environmental factors and/or other diseases. If our hypothesis is confirmed, it will allow differentiation of PPE and SPE sooner than 12weeks postpartum, which is currently the estimated period for confirmation of the specific diagnosis. Furthermore, it could be an early biomarker for predicting the disease, enabling the physician to choose the best clinical management. In addition, it would minimize the use of other methods as the biological sample for obtaining the marker is urine, a practical and effective test with good reproducibility. Finally, test results would enable a greater understanding of the mechanisms involved in gestational hypertension.

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Angiotensin‐converting enzymes 1 and 2 in the feces: presence and catalytic activity in the rat 2,4,6‐trinitrobenzene sulfonic acid‐induced model of colitis

Ferreira‐Duarte,

Oliveira,

Quintas

et al. 2024

J of Gastro and Hepatol

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Background and AimInflammatory bowel disease is challenging to diagnose. Fecal biomarkers offer noninvasive solutions. The renin–angiotensin‐aldosterone system is implicated in intestinal inflammation. Angiotensin‐converting enzyme (ACE) and angiotensin‐converting enzyme 2 (ACE2) regulate its activity, but conflicting findings on these enzymes in colitis require further investigation. We aimed to assess ACE and ACE2 presence and activities in the feces, serum, and colon of 2,4,6‐trinitrobenzene sulfonic acid (TNBS)‐induced rats.MethodsColitis was induced in male rats by rectal instillation of a 21% ethanolic TNBS solution. After rats' sacrifice, colonic portions, serum, and feces were collected. ACE and ACE2 presence in the feces was analyzed by western Blot, and colonic and serum enzymes' concentrations were quantified using ELISA kits. ACE activity was assessed using Hippuryl‐His‐Leu and Z‐Phe‐His‐Leu as substrates. ACE2 activity was assessed using Mca‐APK (Dnp) as a substrate in the presence and absence of DX600 (ACE2 inhibitor).ResultsAn ACE isoform of ~70 kDa was found only in the feces of TNBS‐induced rats. ACE concentration was higher than that of ACE2 in the serum and the inflamed colon. ACE N‐domain activity was higher than that of the C‐domain in all matrices. ACE2 activity was higher in the feces of TNBS‐induced animals compared to controls.ConclusionA 70 kDa ACE isoform only detected in the feces of TNBS‐induced rats may have translational relevance. ACE N‐domain seems to play a significant role in regulating colonic lesions. Further research using human samples is necessary to validate these findings.

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Association of urinary 90 kDa angiotensin- converting enzyme with family history of hypertension and endothelial function in normotensive individuals

Cited by 3 publications

References 22 publications

N-Domain Isoform of Angiotensin I Converting Enzyme as a Marker of Hypertension: Populational Study

N-Domain Isoform of Angiotensin I Converting Enzyme as a Marker of Hypertension: Populational Study

Angiotensin Converting Enzyme 90kDa isoform: Biomarker for diagnosis of preeclampsia?

Angiotensin‐converting enzymes 1 and 2 in the feces: presence and catalytic activity in the rat 2,4,6‐trinitrobenzene sulfonic acid‐induced model of colitis

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