title: Regulation of angiotensin-(1-7) and angiotensin II type 1 receptor by telmisartan and losartan in adriamycin-induced rat heart failure.
abstract: OBJECTIVE
  To investigate the possible effects of telmisartan and losartan on cardiac function in adriamycin (ADR)-induced heart failure in rats, and to explore the changes in plasma level of angiotensin-(1-7)[Ang-(1-7)] and myocardial expression of angiotensin II type 1/2 receptors (AT(1)R / AT(2)R) and Mas receptor caused by the two drugs.
  
  
  METHODS
  Male Sprague-Dawley rats were randomly divided into 4 groups: the control group, ADR-treated heart failure group (ADR-HF), telmisartan plus ADR-treated group (Tel+ADR) and losartan plus ADR-treated group (Los+ADR). ADR was administrated (2.5 mg/kg, ip, 6 times in 2 weeks). The rats in the Tel+ADR and Los+ADR groups were treated orally with telmisartan (10 mg/kg daily po) and losartan (30 mg/kg daily), respectively, for 6 weeks. The plasma level of Ang-(1-7) was determined using ELISA. The mRNA and protein expression of myocardial Mas receptor, AT(1)R and AT(2)R were measured using RT-PCR and Western blotting, respectively.
  
  
  RESULTS
  ADR significantly reduced the plasma level of Ang-(1-7) and the expression of myocardial Mas receptor and myocardial AT(2)R, while significantly increased the expression of myocardial AT(1)R. Treatment with telmisartan and losartan effectively increased the plasma level of Ang-(1-7) and suppressed myocardial AT(1)R expression, but did not influence the expression of Mas receptor and AT(2)R.
  
  
  CONCLUSIONS
  The protective effects of telmisartan and losartan in ADR-induced heart failure may be partially due to regulation of circulating Ang-(1-7) and myocardial AT(1)R expression.
authors.affiliation: Department of Cardiology, First Affiliated Hospital, Nanjing Medical University, China.
authors.forename: Wen-na
authors.initials: WN
authors.lastname: Zong
authors.forename: Xiao-hui
authors.initials: XH
authors.lastname: Yang
authors.forename: Xiu-mei
authors.initials: XM
authors.lastname: Chen
authors.forename: Hong-juan
authors.initials: HJ
authors.lastname: Huang
authors.forename: Hong-jian
authors.initials: HJ
authors.lastname: Zheng
authors.forename: Xiao-yi
authors.initials: XY
authors.lastname: Qin
authors.forename: Yong-hong
authors.initials: YH
authors.lastname: Yong
authors.forename: Kejiang
authors.initials: K
authors.lastname: Cao
authors.forename: Jun
authors.initials: J
authors.lastname: Huang
authors.forename: Xin-zheng
authors.initials: XZ
authors.lastname: Lu
mesh_terms: D000803:Angiotensin I / Q000097:blood* / Q000378:metabolism; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology / Q000627:therapeutic use*; D000818:Animals; D000903:Antibiotics, Antineoplastic / Q000009:adverse effects*; D001562:Benzimidazoles / Q000494:pharmacology / Q000627:therapeutic use*; D001565:Benzoates / Q000494:pharmacology / Q000627:therapeutic use*; D004317:Doxorubicin / Q000009:adverse effects; D005786:Gene Expression Regulation / Q000187:drug effects; D006321:Heart / Q000187:drug effects; D006333:Heart Failure / Q000139:chemically induced / Q000188:drug therapy*; D019808:Losartan / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D009206:Myocardium / Q000378:metabolism; D010446:Peptide Fragments / Q000097:blood* / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics* / Q000378:metabolism; D000077333:Telmisartan
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000903:Antibiotics, Antineoplastic; D001562:Benzimidazoles; D001565:Benzoates; D010446:Peptide Fragments; D044140:Receptor, Angiotensin, Type 1; D004317:Doxorubicin; D000803:Angiotensin I; C118790:angiotensin I (1-7); D019808:Losartan; D000077333:Telmisartan