Distribution of endothelin-1 in the lung of rats with pulmonary hypertension of different etiology

Satoshi Sakai; Takashi Miyauchi; Masahiko Kobayashi; Iwao Yamaguchi; Katsutoshi Goto; Yasuro Sugishita

doi:10.1007/BF01618391

International Journal of Angiology, Table of Contents

Int J Angiol 1998; 7(2): 160-164
DOI: 10.1007/BF01618391

Original Articles

Distribution of endothelin-1 in the lung of rats with pulmonary hypertension of different etiology

Satoshi Sakai¹ , Takashi Miyauchi¹ , Masahiko Kobayashi³ , Iwao Yamaguchi¹ , Katsutoshi Goto² , Yasuro Sugishita¹

¹Cardiovascular Division, Department of Internal Medicine, Institute of Clinical Medicine, University of Tsukuba, Ibaraki, 305-8575, Japan
²Department of Pharmacology, Institute of Basic Medical Sciences, University of Tsukuba, Ibaraki, 305-8575, Japan
³Tsukuba Research Institute, Ibaraki, 300-2671, Japan

Presented at the 38th Annual World Congress, International College of Angiology, Cologne, Germany, June 1996

Abstract

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Abstract

Endothelin (ET)-1 is a potent vasoconstrictor peptide and induces vascular smooth muscle cell proliferation. We previously reported that an ET receptor antagonist prevented the progression of pulmonary hypertension (PH) caused by inflammatory lung disease in rats. The aim of the present study was to investigate whether pathophysiological roles of endogenous ET-1 in PH caused by congestive heart failure (CHF) differ from PH caused by inflammatory lung disease. For this purpose, we investigated the distribution of ET-1 staining (ET-1-like immunoreactivity) by the immunohistochemical method using an anti-ET-1 antibody in the lungs of rats with PH due to CHF or inflammatory lung disease. CHF was surgically induced by permanent left coronary arterial ligation in rats. At 2 weeks after the surgery in rats, left ventricular contractility (LV+dP/dt_max) was decreased, whereas right ventricular systolic pressure was increased, indicating that the rats developed CHF accompanied by PH. The intensity of ET-1 staining was stronger in the pulmonary vascular endothelial cells of the CHF rats than that of the sham-operated rats. We used monocrotaline (MCT)-induced PH rats (MCT rats) as a model of PH due to inflammatory lung disease. Three weeks after MCT injection, the MCT rats developed PH. The intensity of ET-1 staining in the pulmonary vascular endothelial cells of the MCT rats did not differ from that of the control rats, however, the intensity of the ET-1 staining in the MCT rats was increased in the alveolar walls (especially in macrophages). These data show that the distribution of ET-1 staining in the lungs of the rats with PH due to CHF differs from that of the rats with PH due to inflammatory lung disease.

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