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Am J Physiol Heart Circ Physiol 279: H672-H678, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 2, H672-H678, August 2000

Heme oxygenase-1 is upregulated in the rat heart in response to chronic administration of angiotensin II

Nobukazu Ishizaka1,*, Toru Aizawa1,*, Ichiro Mori2, Jun-Ichi Taguchi1, Yoshio Yazaki1, Ryozo Nagai1, and Minoru Ohno1

1 Department of Cardiovascular Medicine, University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8655; and 2 Department of Pathology, Tokai University School of Medicine, Kanagawa 259-1193, Japan

Heme oxygenase (HO) is a heme-catabolizing enzyme that converts heme into biliverdin, iron, and carbon monoxide. HO-1, an inducible form of HO, is thought to act as an endogenous antioxidant defense mechanism. To determine whether chronic administration of angiotensin II affects HO-1 expression in the heart, expression and localization of HO-1 were investigated in the heart of rats receiving angiotensin II infusion (0.7 mg · kg-1 · day-1) via osmotic minipump for up to 7 days. Angiotensin II induced formation of granulation tissue, characterized by myofibroblast proliferation, fibrous deposition, and inflammatory cell migration. Angiotensin II also upregulated cardiac HO-1 expression. Immunohistochemistry revealed that HO-1 was intensively expressed in the granulation tissue. The selective AT1-receptor antagonist, losartan, completely, but hydralazine only partially, suppressed angiotensin II-induced granulation tissue formation and HO-1 upregulation. Chronic norepinephrine infusion (2.8 mg · kg-1 · day-1) did not induce granulation tissue formation or HO-1 upregulation. Our data suggest that angiotensin II upregulates cardiac HO-1 expression in the newly formed inflammatory lesion, which may represent an adaptive response to angiotensin II-induced cardiac damage.

norepinephrine; blood pressure; immunohistochemistry; oxidative stress

* N. Ishizaka and T. Aizawa contributed equally to this paper.




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