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(Hypertension. 2002;39:122.)
© 2002 American Heart Association, Inc.

Scientific Contributions

Regulation and Localization of HSP70 and HSP25 in the Kidney of Rats Undergoing Long-Term Administration of Angiotensin II

Nobukazu Ishizaka; Toru Aizawa; Minoru Ohno; Shin-ichi Usui; Ichiro Mori; Shiow-Shih Tang; Julie R. Ingelfinger; Satoshi Kimura; Ryozo Nagai

From the Departments of Cardiovascular Medicine (N.I., T.A., M.O., S.-I.U., R.N.) and Infection Control and Prevention (S.K.), University of Tokyo, Graduate School of Medicine, Tokyo, Japan; Department of Pathology, Wakayama Medical College (I.M.); and Massachusetts General Hospital (S.-S.T., J.R.I.).

Correspondence to Nobukazu Ishizaka, MD, PhD, Department of Cardiovascular Medicine, University of Tokyo, Graduate School of Medicine, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-8655, Japan. E-mail nobuishizka-tky{at}umin.ac.jp

Various renal insults result in induction of heat shock protein (HSP) expression within the kidney. Some of the HSPs induced in that manner are postulated to have renoprotective effects via either chaperoning actions or antioxidative properties. We have previously reported that long-term angiotensin (Ang) II administration induces the expression of renal HSP32, also known as heme oxygenase-1 (HO-1). Here, we investigated the regulation of expression and localization of other HSPs, including HSP70, HSP25, and B-crystallin, in the kidney of rats undergoing long-term administration of Ang II (0.7 mg · kg^-1 · d^-1). Immunoblot analysis demonstrated that Ang II increased renal expression of HSP70 and HSP25, as well as HO-1, but that expression of B-crystallin was unaffected by this treatment. The Ang II–induced increase in renal HSP70 and HSP25 was dependent on the angiotensin type 1 receptor activation but not on hypertension per se. Immunohistochemistry revealed that HSP70 and HSP25 were expressed in the medullar regions and in the renal arterial wall in the kidney of control rats. After Ang II infusion, signals for HSP70, HSP25, and HO-1 proteins increased in intensity in the endothelium and medial smooth muscle of the renal artery. In addition, all of these HSPs were induced in proximal renal tubular epithelial cells from the same segments, suggesting that similar mechanisms are responsible for upregulating these HSPs. Our data show that Ang II infusion induces renal HSP70 and HSP25, as well as HO-1, and that Ang II can induce expression of these HSPs in renal cells in a pressor-independent manner.

Key Words: angiotensin • AT₁ receptor • hypertension • heat shock protein • kidney

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