Imbalanced plasma ACE and ACE2 level in the uremic patients with cardiovascular diseases and its change during a single hemodialysis session

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Abstract

Background: The renin-angiotensin system (RAS) has significant influences on heart and renal disease progression. Angiotensin converting enzyme (ACE) and angiotensin converting enzyme II (ACE2) are major peptidases of RAS components and play counteracting functions through angiotensin II (Ang II)/ATIR and angiotensin-(1–7) (Ang-(1–7))/Mas axis, respectively.

Methods: There were 360 uremic patients on regular hemodialysis (HD) treatment (inclusive of 119 HD patients with cardiovascular diseases (CVD) and 241 HD patients without CVD and 50 healthy subjects were enrolled in this study. Plasma ACE, ACE2, Ang II and Ang-(1–7) levels of the HD patients were determined.

Results: We compared pre-HD levels of plasma ACE, ACE2, Ang II and Ang-(1–7) in the HD patients with and without CVD to those of the controls. The HD patients, particularly those with CVD, showed a significant increase in the levels of ACE and Ang II, whereas ACE2 and Ang-(1–7) levels were lower than those in the healthy controls. Therefore, imbalanced ACE/ACE2 was observed in the HD patients with CVD. In the course of a single HD session, the plasma ACE, ACE/ACE2 and Ang II levels in the HD patients with CVD were increased from pre-HD to post-HD. On the contrary, ACE2 levels were decreased after the HD session. These changes were not detected in the HD patients without CVD.

Conclusions: Pathogenically imbalanced circulating ACE/ACE2 was detected in the HD patients, particularly those with CVD. HD session could increase ACE/Ang II/AT1R axis and decrease ACE2/Ang-(1–7)/Mas axis activity in the circulation of HD patients with CVD.

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Most cited references 37

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Cardiovascular disease in chronic kidney disease. A clinical update from Kidney Disease: Improving Global Outcomes (KDIGO).

Charles Herzog, Richard W Asinger, Alan K Berger … (2011)

Cardiovascular morbidity and mortality in patients with chronic kidney disease (CKD) is high, and the presence of CKD worsens outcomes of cardiovascular disease (CVD). CKD is associated with specific risk factors. Emerging evidence indicates that the pathology and manifestation of CVD differ in the presence of CKD. During a clinical update conference convened by the Kidney Disease: Improving Global Outcomes (KDIGO), an international group of experts defined the current state of knowledge and the implications for patient care in important topic areas, including coronary artery disease and myocardial infarction, congestive heart failure, cerebrovascular disease, atrial fibrillation, peripheral arterial disease, and sudden cardiac death. Although optimal strategies for prevention, diagnosis, and management of these complications likely should be modified in the presence of CKD, the evidence base for decision making is limited. Trials targeting CVD in patients with CKD have a large potential to improve outcomes.

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Angiotensin-converting enzyme 2, angiotensin-(1-7) and Mas: new players of the renin-angiotensin system.

Robson A S Santos, Anderson J. Ferreira, Thiago Verano-Braga … (2013)

Angiotensin (Ang)-(1-7) is now recognized as a biologically active component of the renin-angiotensin system (RAS). Ang-(1-7) appears to play a central role in the RAS because it exerts a vast array of actions, many of them opposite to those attributed to the main effector peptide of the RAS, Ang II. The discovery of the Ang-converting enzyme (ACE) homolog ACE2 brought to light an important metabolic pathway responsible for Ang-(1-7) synthesis. This enzyme can form Ang-(1-7) from Ang II or less efficiently through hydrolysis of Ang I to Ang-(1-9) with subsequent Ang-(1-7) formation by ACE. In addition, it is now well established that the G protein-coupled receptor Mas is a functional binding site for Ang-(1-7). Thus, the axis formed by ACE2/Ang-(1-7)/Mas appears to represent an endogenous counterregulatory pathway within the RAS, the actions of which are in opposition to the vasoconstrictor/proliferative arm of the RAS consisting of ACE, Ang II, and AT(1) receptor. In this brief review, we will discuss recent findings related to the biological role of the ACE2/Ang-(1-7)/Mas arm in the cardiovascular and renal systems, as well as in metabolism. In addition, we will highlight the potential interactions of Ang-(1-7) and Mas with AT(1) and AT(2) receptors.

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Circulating ACE2 activity is increased in patients with type 1 diabetes and vascular complications.

Aino Soro-Paavonen, Daniel Gordin, Carol Forsblom … (2012)

Angiotensin-converting enzyme 2 (ACE2) is a homolog of ACE that counterbalances the actions of angiotensin (AT)II and promotes vasodilatation. Circulating ACE2 activity is increased in diabetes in experimental models. The role of ACE2 in human pathophysiology is unknown. We examined whether ACE2 activity is altered in patients with type 1 diabetes (T1D), with and without diabetic nephropathy. Quantitative ACE2 activity in serum was measured by a fluorometric assay in 859 patients with T1D in the Finnish Diabetic Nephropathy (FinnDiane) study and in 204 healthy controls. Pulse-wave analysis with augmentation index (AIx) measurement was performed in 319 patients with T1D and 114 controls. ACE2 activity was increased in men with T1D and microalbuminuria (30.2 ± 1.5 ngE/ml) when compared to patients without albuminuria (27.0 ± 0.5 ngE/ml, P < 0.05) or controls (25.6 ± 0.8 ngE/ml, P < 0.05). ACE2 activity was increased in male and female patients who were on ACE inhibitor (ACEi) treatment, also independently of albuminuria. Male and female patients with coronary heart disease (CHD) had significantly increased ACE2 activity (35.5 ± 2.5 vs. 27.0 ± 0.5 ngE/ml, P < 0.001 among male T1D patients vs. male controls). ACE2 activity correlated positively with systolic blood pressure (rs = 0.175, P < 0.001), AIx (rs = 0.191, P = 0.010) and diabetes duration (rs = 0.198, P < 0.001), and negatively with estimated glomerular filtration rate (rs = -0.109, P = 0.016) among male T1D patients. ACE2 activity increases with increasing vascular tone and when the patient with T1D has microvascular or macrovascular disease, indicating that ACE2 may participate as a compensatory mechanism in the regulation of vascular and renal function in patients with T1D.

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Author and article information

Journal

Journal ID (nlm-ta): Ren Fail

Journal ID (iso-abbrev): Ren Fail

Journal ID (publisher-id): IRNF

Journal ID (publisher-id): irnf20

Title: Renal Failure

Publisher: Taylor & Francis

ISSN (Print): 0886-022X

ISSN (Electronic): 1525-6049

Publication date Collection: 2017

Publication date (Electronic): 20 November 2017

Volume: 39

Issue: 1

Pages: 719-728

Affiliations

[a ]Department of Biological Science and Technology, National Chiao Tung University , Hsinchu, Taiwan;

[b ]Division of Nephrology, Department of Internal Medicine, National Taiwan University Hospital Hsinchu Branch , Hsinchu, Taiwan;

[c ]Division of Nephrology, Department of Internal Medicine, Shin Kong Wu Ho-Su Memorial Hospital , Taipei, Taiwan;

[d ]Division of Nephrology, Department of Internal Medicine, Changhua Christian Hospital , Changhua, Taiwan;

[e ]School of Medicine, Chung-Shan Medical University , Taichung, Taiwan;

[f ]Division of Chest Medicine, Department of Internal Medicine, Hsinchu Mackay Memorial Hospital , Hsinchu, Taiwan;

[g ]Department of Senior Citizen Service Management, Minghsin University of Science and Technology , Hsinchu, Taiwan

Author notes

[*]

This author contributed equally to the first author.

Supplemental data for this article can be accessed here .

CONTACT Chih-Sheng Lin lincs@ 123456mail.nctu.edu.tw Department of Biological Science and Technology, National Chiao Tung University , No.75 Po-Ai Street, Hsinchu30068, Taiwan

Author information

Chung-Wei Yang http://orcid.org/0000-0002-8613-3597

Ching-Chang Cho http://orcid.org/0000-0002-5087-3542

Chih-Sheng Lin http://orcid.org/0000-0002-1609-7594

Article

Publisher ID: 1398665

DOI: 10.1080/0886022X.2017.1398665

PMC ID: 6446170

PubMed ID: 29157100

SO-VID: 6e6ed76a-3ba8-4a30-a6ed-1e4912a278db

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 11 April 2017

Date revision received : 14 September 2017

Date accepted : 23 October 2017

Page count

Pages: 10, Words: 7181

Funding

Funded by: Ministry of Science and Technology

Award ID: MMH-CT-10503

Award ID: MMH-HB-10507

Funded by: Hsinchu Mackay Memorial Hospital 10.13039/501100004861

Funded by: .

This work was supported by the grant of MOST 104-2313-B-009-001-MY3 from the Ministry of Science and Technology (MOST), Taiwan. This work is also supported by the grands of MMH-CT-10503 and MMH-HB-10507 from the Hsinchu Mackay Memorial Hospital, Taiwan.

Imbalanced plasma ACE and ACE2 level in the uremic patients with cardiovascular diseases and its change during a single hemodialysis session

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Karger: Nephrology

Most cited references 37

Cardiovascular disease in chronic kidney disease. A clinical update from Kidney Disease: Improving Global Outcomes (KDIGO).

Angiotensin-converting enzyme 2, angiotensin-(1-7) and Mas: new players of the renin-angiotensin system.

Circulating ACE2 activity is increased in patients with type 1 diabetes and vascular complications.

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