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Am J Physiol Regul Integr Comp Physiol 277: R1321-R1330, 1999;
0363-6119/99 $5.00
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Vol. 277, Issue 5, R1321-R1330, November 1999

Effects of physiological or pathological pressure load in vivo on myocardial expression of ET-1 and receptors

Michihiko Ueno1, Takashi Miyauchi1,2, Satoshi Sakai1, Tsutomu Kobayashi1, Katsutoshi Goto2,3, and Iwao Yamaguchi1

1 Cardiovascular Division, Department of Internal Medicine, Institute of Clinical Medicine, 3 Department of Pharmacology, Institute of Basic Medical Sciences, and 2 Center for Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan

Endothelin (ET)-1 has potent positive inotropic and chronotropic activity in the heart and induces cardiac hypertrophy. The production of ET-1 in the heart is reported to be increased under some conditions. In normal circulation, the pressure load to the left ventricle (LV) is much greater than that to the right ventricle (RV). In this study, we investigated the gene expression of the myocardial ET-1 system (ET-1, ETA receptor, and ETB receptor) in the RV and LV of normal rats and also investigated these genes in hypertrophied RV due to pathological pulmonary hypertension (PH). Normal rats showed no differences between the RV and LV in the gene expression of either ET-1, ETA receptor, or ETB receptor in either the adult stage (11 wk old) or the neonatal stage (1 and 8 days old). On the other hand, the expression of both atrial natriuretic peptide (ANP) mRNA and B-type natriuretic peptide (BNP) mRNA was significantly greater in the LV than in the RV in adult rats. Gene expression of ET-1, ETA receptor, and ETB receptor in the RV was markedly higher in rats with monocrotaline-induced (pathological) PH than that in control rats. The expression of ANP mRNA and BNP mRNA in the RV was also markedly higher in the rats with PH. In conclusion, the data suggest that gene expression of the ET-1 system in the myocardium is not affected by physiological pressure load in either the adult stage or neonatal stage; however, it is enhanced by pathological pressure overload such as that in PH.

myocardial endothelin-1 system; pressure overload; pulmonary hypertension; cardiac hypertrophy; atrial natriuretic peptide; B-type natriuretic peptide


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