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Volume 332, Issue 1-2 p. 31-34
Research letters
Free Access

Increased production of endothelin-1 in the hypertrophied rat heart due to pressure overload

Ryosuke Yorikane

Ryosuke Yorikane

Department of Pharmacology, Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba, Ibaraki 305, Japan

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Satoshi Sakai

Satoshi Sakai

Department of Pharmacology, Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba, Ibaraki 305, Japan

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Takashi Miyauchi

Takashi Miyauchi

Department of Internal Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki 305, Japan

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Takeshi Sakurai

Takeshi Sakurai

Department of Pharmacology, Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba, Ibaraki 305, Japan

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Yasuro Sugishita

Yasuro Sugishita

Department of Internal Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki 305, Japan

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Katsutoshi Goto

Katsutoshi Goto

Department of Pharmacology, Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba, Ibaraki 305, Japan

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First published: October 11, 1993
Citations: 96
Corresponding author. Fax: (81) (298) 533 039.

Abstract

Endothelin-1 (ET-1) has been demonstrated to induce hypertrophy in cultured cardiac myocytes. We investigated the production of ET-1 in the heart of aorta-banded rats in vivo. Seven days after the banding of the abdominal aorta, rats developed a significant left ventricular hypertrophy. The tissue content of mature ET-1 and the level of expression of prepro ET-1 mRNA were higher in the left ventricle of aorta-banded rats than in those of sham-operated rats. The expression of prepro ET-1 mRNA in the right ventricle was not different between the two groups. These findings indicate that the production of ET-1 increased in the hypertrophied left ventricle, thereby suggesting the possible involvement of endogenous ET-1 in the development of cardiac hypertrophy due to pressure overload.