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Cardiovascular Research 2000 46(1):73-81; doi:10.1016/S0008-6363(00)00008-0
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Type 2 angiotensin II receptor is downregulated in cardiomyocytes of patients with heart failure

Toshiyuki Matsumotoa, Ryoji Ozonoa,*, Tetsuya Oshimaa, Hideo Matsuurab, Taijiro Suedac, Goro Kajiyamab and Masayuki Kambea

aDepartment of Clinical Laboratory Medicine, Hiroshima University School of Medicine, Hiroshima, Japan
bFirst Department of Internal Medicine, Hiroshima University School of Medicine, Hiroshima, Japan
cFirst Department of Surgery, Hiroshima University School of Medicine, Hiroshima, Japan

* Corresponding author. Tel.: +81-82-257-5552; fax: +81-82-257-5554 fwga3144{at}mb.infoweb.ne.jp

Background: The human heart expresses type 2 angiotensin (AT2) receptor, but the function is poorly defined. Methods: In the present study, we investigated (1) the cellular localization of the AT2 receptor and (2) the relationship between the AT2 receptor protein expression and the cardiac function of patients with ischemic heart disease. The receptor localization was assessed by immunohistochemistry and the protein expression was quantified by Western blotting in atrial tissues freshly obtained from 22 patients undergoing coronary artery bypass graft surgery (63.0±11.0 years old; male ratio, 85%). Prior to the surgery, blood was drawn for determination of atrial-natriuretic hormone level and the left ventricular function was assessed by ultrasound cardiography. Results: The results of immunohistochemistry showed that the AT2 receptor was localized to cardiomyocytes and was not present in fibroblasts, vascular smooth muscles, or vascular endothelium. Atrial tissues showed various degrees of structural remodeling, but the localization of the AT2 receptor was not altered in any tissue sections. The amount of the AT2 receptor was negatively correlated with end-diastolic left ventricular diastolic dimension (r=–0.56, P<0.01), calculated left ventricular mass index (r=–0.51, P<0.02) and the plasma atrial natriuretic peptide (ANP) concentration (r=–0.62, P<0.01) and positively correlated with left ventricular ejection fraction (r=0.48, P<0.05). Conclusions: (1) The AT2 receptor is localized to cardiomyocytes independently of the cardiac function. (2) Left ventricular dysfunction is associated with decreased expression of myocardial AT2 receptor protein.

KEYWORDS Angiotensin; Fibrosis; Ischemia; Heart failure; Receptors; Coronary disease; Myocytes; Ventricular function


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