On angiotensin II receptor distribution after myocardial infarction in dogs.
- Author:
Xiu-fen QU
1
;
Jing-jie LI
;
Yang XI
;
Jing-xia SHEN
;
Chun-hong XIU
;
Le YUE
;
Gui-zhao WANG
;
Yong-lin HUANG
Author Information
- Publication Type:Journal Article
- MeSH: Angiotensin II Type 1 Receptor Blockers; pharmacology; therapeutic use; Animals; Dogs; Female; Male; Myocardial Infarction; drug therapy; metabolism; physiopathology; Myocardium; metabolism; RNA, Messenger; metabolism; Receptor, Angiotensin, Type 1; metabolism; Receptor, Angiotensin, Type 2; metabolism; Tetrazoles; pharmacology; therapeutic use; Valine; analogs & derivatives; pharmacology; therapeutic use; Valsartan
- From: Chinese Journal of Cardiology 2009;37(4):358-362
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of valsartan on expression of angiotensin II receptors in different regions of heart after myocardial infarction (MI).
METHODSCanines were divided into sham-operated control group (n=7), infarction group (n=7) and Valsartan group (10 mg x kg(-1) x day(-1) for 4 weeks after MI operation, n=7). Four weeks after operation, Doppler tissue imaging (DTI) was used to evaluate regional ventricular function in the noninfarcted myocardium (apical and basal near to the infarction region). The mRNA and protein expressions of angiotensin II type 1 receptor (AT1-R) and angiotensin II type 2 receptor (AT2-R) on the corresponding regions were detected by competitive reverse-transcriptase polymerase chain reaction technique and immunohistochemical technique respectively. Results The protein and mRNA expressions of AT1-R were significantly increased in both apical and basal regions near to the infarction in dogs with MI compared with those in control group (P < 0.05) which could be downregulated by valsartan (P < 0.05). AT2-R expressions were significantly upregulated in infarction group in both apical and basal regions compared with those in control group and valsartan further increased AT2-R expressions in both areas (P < 0.05). Myocardial peak systolic velocity (Sm), myocardial peak early diastolic velocity (Em) and myocardial peak late diastolic velocity (Am) at both apical and basal regions near to the infarction regions were significantly lower in MI group than those in the control group which could be significantly improved by valsartan.
CONCLUSIONBoth mRNA and protein expressions of AT1-R and AT2-R are upregulated in noninfarcted regions near MI, valsartan improved myocardial function via inhibiting AT1-R upregulation and enhancing AT2-R upregulation.