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Circulation. 1997;96:3954-3962

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(Circulation. 1997;96:3954-3962.)
© 1997 American Heart Association, Inc.

Articles

Angiotensin Type 2 Receptors Are Reexpressed by Cardiac Fibroblasts From Failing Myopathic Hamster Hearts and Inhibit Cell Growth and Fibrillar Collagen Metabolism

Naohiko Ohkubo, MD; Hiroaki Matsubara, MD, PhD; Yoshihisa Nozawa, PhD; Yasukiyo Mori, MD, PhD; Satoshi Murasawa, MD, PhD; Kazuhisa Kijima, MD; Katsuya Maruyama, MD; Hiroya Masaki, MD, PhD; Yoshiaki Tsutumi, MD; Yoshinobu Shibazaki, MD; Toshiji Iwasaka, MD, PhD; ; Mitsuo Inada, MD, PhD

From the Department of Medicine II, Kansai Medical University, Osaka, and the Pharmacological Laboratory, Taiho Pharmaceutical Co, Ltd, Tokushima (Y.N.), Japan.

Correspondence to Hiroaki Matsubara, MD, Department of Medicine II, Kansai Medical University, Fumizonocho 10-15, Moriguchi, Osaka 570, Japan. E-mail matsubah{at}takii.kmu.ac.jp

Background Angiotensin (Ang) II type 1 receptor (AT1-R) induces cardiomyocyte hypertrophy and fibroblast proliferation, whereas the physiological role of AT2-R in cardiac remodeling remains poorly defined.

Methods and Results Using Bio14.6 cardiomyopathic (CM) hamsters, we found that AT2-R sites were increased by 153% during heart failure compared with F1B controls. AT1-R numbers were increased by 72% in the hypertrophy stage and then decreased to the control level during heart failure. Such differential regulation of AT2-R and AT1-R during heart failure was consistent with changes in the respective mRNA levels. Autoradiography and immunocytochemistry revealed that both AT2-R and AT1-R are localized at higher densities in fibroblasts present in fibrous regions. Surrounding myocardium predominantly expressed AT1-R, but the level of expression was less than that in fibrous regions. Cardiac fibroblasts isolated from CM hearts during heart failure but not from control hamsters expressed AT2-R (30 fmol/mg protein). Using the cardiac fibroblasts expressing AT2-R, we found that Ang II stimulated net collagenous protein production by 48% and pretreatment with an AT2-R antagonist, PD123319, evoked a further elevation (83%). Ang II–induced synthesis of fibronectin and collagen type I were enhanced by 40% and 53%, respectively, by pretreatment with PD123319. Ang II–induced DNA synthesis (assessed by [3H]thymidine uptake) was significantly increased by PD123319, and the AT2-R agonist CGP42112A reduced the serum-stimulated increase in cell numbers by 23%. Treatment with an AT1-R antagonist, TCV116, for 20 weeks inhibited progression of interstitial fibrosis by 28%, whereas with 44-week PD123319 treatment but not 20-week treatment, the extent of the fibrous region was increased significantly, by 29%.

Conclusions These findings demonstrate that AT2-R is reexpressed by cardiac fibroblasts present in fibrous regions in failing CM hearts and that the increased AT2-R exerts an anti–AT1-R action on the progression of interstitial fibrosis during cardiac remodeling by inhibiting both fibrillar collagen metabolism and growth of cardiac fibroblasts.


Key Words: angiotensin • receptors • remodeling • cardiomyopathy • cells




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