Journal
ARCHIVES OF CARDIOVASCULAR DISEASES
Volume 106, Issue 4, Pages 196-201Publisher
ELSEVIER MASSON
DOI: 10.1016/j.acvd.2013.01.004
Keywords
Hypertension; Angiotensin-converting enzyme 2; Angiotensin-converting enzyme inhibitors; Enalapril
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Background. - The discovery of angiotensin-converting enzyme 2 (ACE2) has greatly modified understanding of the renin-angiotensin system (RAS). Aims. - To investigate the cardiac expression of ACE2 and ACE in spontaneously hypertensive rats (SHRs) and the effects of enalapril on them. Methods. - Fifteen SHRs were randomly assigned to two groups: an SHR control group (n = 7), treated with vehicle; and an enalapril group (n = 8), treated with enalapril (15 mg/kg/day). After 4 weeks of treatment, the rats were killed and the left ventricular tissue was dissected. Reverse transcription-polymerase chain reaction and Western blot protein staining were performed to detect expression of ACE2 and ACE messenger ribonucleic acid (mRNA) and protein. Ten Wistar Kyoto rats (WKYs) served as the normotensive control group, which were treated with vehicle. Results. - Compared with in normotensive WKYs, cardiac expression of ACE mRNA and protein in SHRs was increased (1.68 +/- 0.34 vs. 0.33 +/- 0.12, P < 0.05 and 1.21 +/- 0.14 vs. 0.71 +/- 0.11, P < 0.05, respectively), whereas cardiac expression of ACE2 mRNA and protein was decreased (0.50 +/- 0.15 vs. 1.16 +/- 0.24, P < 0.05 and 0.71 +/- 0.24 vs. 1.22 +/- 0.14, P < 0.05, respectively). After treatment with enalapril, the levels of ACE mRNA and protein were decreased (0.44 +/- 0.19 vs. 1.68 +/- 0.34, P < 0.01 and 0.87 +/- 0.13 vs. 1.21 +/- 0.14, P < 0.05, respectively), the level of ACE2 mRNA was increased (1.77 +/- 0.49 vs. 0.50 +/- 0.15, P < 0.05) but the level of ACE2 protein remained unchanged. Conclusions. - In SHRs, the expression of cardiac ACE was remarkably increased, whereas ACE2 was notably decreased. Reduction of ACE and elevation of ACE2 might be one of the mechanisms underlying the antihypertensive function of enalapril. (C) 2013 Elsevier Masson SAS. All rights reserved.
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