Abstract | INTRODUCTION: MATERIALS AND METHODS: RESULTS:
Hydronephrosis led to an increase of ACE level and a decrease of ACE2 and Mas receptor in the heart. Losartan decreased cardiac ACE level, but ACE2 and Mas receptor levels significantly increased in hydronephrotic mice (p < 0.01). Enalapril increased ACE2 levels (p < 0.01), but did not affect Mas receptor in the heart. Plasma renin activity (PRA) and Ang II decreased in hydronephrotic mice, but significantly increased after treatment with losartan or enalapril. CONCLUSIONS:
Hydronephrosis increased cardiac ACE and suppressed ACE2 and Mas receptor levels. AT1 blockade caused sustained activation of cardiac ACE2 and Mas receptor, but ACE inhibitor had the limitation of such activation of Mas receptor in hydronephrotic animals.
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Authors | Yanling Zhang, Lulu Ma, Junyan Wu, Tingting Chen |
Journal | Journal of the renin-angiotensin-aldosterone system : JRAAS
(J Renin Angiotensin Aldosterone Syst)
Vol. 16
Issue 2
Pg. 267-74
(Jun 2015)
ISSN: 1752-8976 [Electronic] England |
PMID | 25650385
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | © The Author(s) 2015. |
Chemical References |
- Angiotensins
- Proto-Oncogene Mas
- Proto-Oncogene Proteins
- Receptors, G-Protein-Coupled
- Peptidyl-Dipeptidase A
- Ace2 protein, mouse
- Angiotensin-Converting Enzyme 2
- Renin
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Topics |
- Angiotensin-Converting Enzyme 2
- Angiotensins
(blood)
- Animals
- Blood Pressure
- Body Weight
- Hydronephrosis
(blood, enzymology, pathology, physiopathology)
- Male
- Mice, Inbred BALB C
- Myocardium
(enzymology, pathology)
- Organ Size
- Peptidyl-Dipeptidase A
(genetics, metabolism)
- Proto-Oncogene Mas
- Proto-Oncogene Proteins
(genetics, metabolism)
- Receptors, G-Protein-Coupled
(genetics, metabolism)
- Renin
(blood)
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