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(Hypertension. 2002;40:853.)
© 2002 American Heart Association, Inc.

Scientific Contributions

Effect of AT₂ Receptor on Expression of AT₁ and TGF-ß Receptors in VSMCs from SHR

Jin-Zi Su; Noboru Fukuda; Xue-Qing Jin; Yi-Mu Lai; Ryo Suzuki; Yoshiko Tahira; Hiroto Takagi; Yukihiro Ikeda; Katsuo Kanmatsuse; Hitoshi Miyazaki

From the Second Department of Internal Medicine, Nihon University School of Medicine (J.-Z.S., N.F., X.-Q.J., Y.-M.L., R.S., Y.T., H.T., Y.I., K.K.), Tokyo, Japan; and Gene Experiment Center, University of Tsukuba (H.M.), Ibaraki, Japan.

Correspondence to Noboru Fukuda, MD, PhD, Second Department of Internal Medicine, Nihon University School of Medicine, Ooyaguchi-kamimachi 30-1, Itabashi-ku, Tokyo 173-8610, Japan. E-mail nhukuda{at}med.nihon-u.ac.jp

We recently reported that overexpression of the angiotensin II type 2 (AT₂) receptor downregulates the AT_1a receptor through the bradykinin/NO pathway in a ligand-independent manner in vascular smooth muscle cells (VSMCs). In the present study, we investigated the effect of AT₂ receptor overexpression on the expression of the AT_1a receptor and transforming growth factor-ß (TGF-ß) receptor subtypes in VSMCs from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Transfection of the AT₂ receptor gene downregulated expression of the AT_1a receptor in VSMCs from WKY, but did not affect expression of the AT_1a receptor in VSMCs from SHR. Transfection of the AT₂ receptor abolished DNA synthesis in response to angiotensin II in VSMCs from WKY; in VSMCs from SHR, basal DNA synthesis was suppressed, but DNA synthesis in response to Ang II was not altered. The NO substrate L-arginine augmented downregulation of the AT_1a receptor in VSMCs from WKY, whereas it did not affect expression of the AT_1a receptor in VSMCs from SHR. In response to AT₂ receptor transfection, expression of TGF-ß type I receptor mRNA was suppressed significantly in VSMCs from WKY, whereas expression of TGF-ß type I receptor was not altered in VSMCs from SHR. These results suggest that the AT₂ receptor downregulates AT_1a and TGF-ß type I receptors in normal VSMCs, but not in SHR-derived VSMCs. The lack of downregulation of the AT_1a receptor may contribute, in part, to the exaggerated growth of VSMCs from SHR.

Key Words: receptors, angiotensin II • muscle, smooth, vascular • rats, spontaneously hypertensive

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