title: Hydronephrosis alters cardiac ACE2 and Mas receptor expression in mice.
abstract: BACKGROUND
  Hydronephrosis is characterized by substantial loss of tubules and affects renin secretion in the kidney. However, whether alterations of angiotensin-converting enzyme (ACE), ACE2 and Mas receptor in the heart are observed in hydronephrosis is unknown. Thus, we assessed these components in hydronephrotic mice treated with AT1 receptor blockade and ACE inhibitor.
  
  
  METHODS
  Hydronephrosis was induced by left ureteral ligation in Balb/C mice except sham-operated animals. The levels of cardiac ACE, ACE2 and Mas receptor were measured after treatment of losartan or enalapril.
  
  
  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.
authors: Department of Physiology, Institute of Neurobiology, Taishan Medical University, China lzhang98@hotmail.com.
authors: Yanling
authors: Y
authors: Zhang
authors: Department of Physiology, Institute of Neurobiology, Taishan Medical University, China.
authors: Lulu
authors: L
authors: Ma
authors: Department of Physiology, Institute of Neurobiology, Taishan Medical University, China.
authors: Junyan
authors: J
authors: Wu
authors: Department of Physiology, Institute of Neurobiology, Taishan Medical University, China.
authors: Tingting
authors: T
authors: Chen
mesh_terms: D000085962:Angiotensin-Converting Enzyme 2; D000809:Angiotensins / Q000097:blood; D000818:Animals; D001794:Blood Pressure; D001835:Body Weight; D006869:Hydronephrosis / Q000097:blood / Q000201:enzymology* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008807:Mice, Inbred BALB C; D009206:Myocardium / Q000201:enzymology* / Q000473:pathology; D009929:Organ Size; D007703:Peptidyl-Dipeptidase A / Q000235:genetics / Q000378:metabolism; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000378:metabolism*; D043562:Receptors, G-Protein-Coupled / Q000235:genetics / Q000378:metabolism*; D012083:Renin / Q000097:blood
chemical_list: D000809:Angiotensins; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins; D043562:Receptors, G-Protein-Coupled; D007703:Peptidyl-Dipeptidase A; C000705328:Ace2 protein, mouse; D000085962:Angiotensin-Converting Enzyme 2; D012083:Renin
keywords: ACE inhibitor; AT1 receptor; Hydronephrosis; heart; kidney; renin