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(Hypertension. 1999;33:975-980.)
© 1999 American Heart Association, Inc.

Scientific Contributions

Angiotensin II Type 1 Receptor Antagonist Downregulates Nonmuscle Myosin Heavy Chains in Spontaneously Hypertensive Rat Aorta

Kozo Fujii; Seiji Umemoto; Akihisa Fujii; Takahito Yonezawa; Toshihiro Sakumura; Masunori Matsuzaki

From the Second Department of Internal Medicine, Yamaguchi University School of Medicine, Ube, Yamaguchi, Japan.

Correspondence to Masunori Matsuzaki, MD, PhD, 2nd Department of Internal Medicine, Yamaguchi University School of Medicine, 1144 Kogushi, Ube, Yamaguchi 755-8505, Japan. E-mail masunori{at}po.cc.yamaguchi-u.ac.jp

Abstract—The aim of this study was to clarify the differences between the angiotensin II type 1 (AT₁) receptor antagonist and the angiotensin-converting enzyme (ACE) inhibitor on smooth muscle and nonmuscle myosin heavy chain isoforms in aortic smooth muscle cells of Wistar-Kyoto rats and spontaneously hypertensive rats. All 4 myosin heavy chain isoforms are heterogeneously expressed in the smooth muscle cells of the aortic tunica media in 20-week-old rats, and the contractile-type myosin heavy chains are highly expressed in smooth muscle cells of the aortic tunica media compared with the synthetic-type myosin heavy chains. Both the AT₁ receptor antagonist and the ACE inhibitor had the same effects on hemodynamics, smooth muscle cell hypertrophy and proliferation, fibrosis, and vascular remodeling in spontaneously hypertensive rats. However, the AT₁ receptor antagonist had a more potent effect on the downregulation of the synthetic-type myosin heavy chains than the ACE inhibitor in spontaneously hypertensive rat aortic tunica media. In contrast, these effects of the AT₁ receptor antagonist and the ACE inhibitor on hemodynamics, morphology, fibrosis, and expression of myosin heavy chain isoforms in smooth muscle cells of the aortic tunica media were not observed in Wistar-Kyoto rats. Thus, within 6 weeks, the AT₁ receptor antagonist might modulate the cellular composition of myosin heavy chain isoforms in smooth muscle cells more efficiently than the ACE inhibitor, without morphological changes in the spontaneously hypertensive rat aorta.

Key Words: angiotensin • aorta • hypertension, arterial • muscle, smooth • myosin

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