Cardiac and renal distribution of ACE and ACE-2 in rats with heart failure

Ravit Cohen-Segev, Bahaa Francis, Niroz Abu-Saleh, Hoda Awad, Aviva Lazarovich, Aviva Kabala, Doron Aronson, Zaid Abassi

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

Congestive heart failure is often associated with impaired kidney function. Over-activation of the renin-angiotensin-aldosterone system (RAAS) contributes to avid salt and water retention in heart failure. While the expression of angiotensin converting enzyme (ACE), a key enzyme in the synthesis of angiotensin II (Ang II), is well established, the expression of angiotensin converting enzyme-2 (ACE-2), an enzyme responsible for angiotensin 1-7 generation, is largely unknown. This issue is of a special interest since angiotensin 1-7 counteracts many of the proliferative and hypertensive effects of angiotensin II. Therefore, the present study was designed to investigate the expression of both enzymes in the kidney and heart of rats with heart failure. Heart failure (CHF) was induced in male Sprague Dawley rats (. n=. 9) by the creation of a surgical aorto-caval fistula. Sham-operated rats served as controls (. n=. 8). Two weeks after surgery, the animals were sacrificed and their hearts and kidneys were harvested for assessment of cardiac remodeling and ACE and ACE-2 immunoreactivity by immunohistochemical staining. ACE immunostaining was significantly increased in the kidneys (4.34. ±. 0.39% vs. 2.96. ±. 0.40%, P<. 0.05) and hearts (4.57. ±. 0.54% vs. 2.19. ±. 0.37%, P<. 0.01) of CHF rats as compared with their sham controls. In a similar manner, ACE-2 immunoreactivity was also elevated in the kidneys (4.65. ±. 1.17% vs. 1.75. ±. 0.29%, P<. 0.05) and hearts (5.48. ±. 1.11% vs. 1.13. ±. 0.26%, P<. 0.01) of CHF rats as compared with their healthy controls. This study showed that both ACE and ACE-2 are overexpressed in the cardiac and renal tissues of animals with heart failure as compared with their sham controls. The increased expression of the beneficial ACE-2 in heart failure may serve as a compensatory response to the over-activity of the deleterious isoform, namely, angiotensin converting enzyme 1(ACE-1).

Original languageEnglish
Pages (from-to)1342-1349
Number of pages8
JournalActa Histochemica
Volume116
Issue number8
DOIs
StatePublished - 1 Oct 2014
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2014 Elsevier GmbH.

Funding

This study was supported by the Jess and Mildred Fisher Family Cardiology Research Fund (No. 2016879 ), Technion – Israeli Institute of Technology .

FundersFunder number
Technion – Israeli Institute of Technology
Jess and Mildred Fisher Center for Familial Cancer Research2016879

    Keywords

    • Angiotensin 1-7
    • Angiotensin II
    • Angiotensin converting enzyme
    • Angiotensin converting enzyme 2
    • Heart failure
    • Kidney
    • Rat

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