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J Appl Physiol 94: 446-452, 2003. First published October 4, 2002; doi:10.1152/japplphysiol.00239.2002
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Vol. 94, Issue 2, 446-452, February 2003

Effects of ET-A receptor blockade on eNOS gene expression in chronic hypoxic rat lungs

Friedrich C. Blumberg1, Konrad Wolf2, Michael Arzt1, Cornelia Lorenz1, Günter A. J. Riegger1, and Michael Pfeifer1

1 Department of Internal Medicine II, and 2 Institute of Physiology, University of Regensburg, 93042 Regensburg, Germany

We tested the hypothesis that pulmonary endothelial nitric oxide synthase (eNOS) gene expression is primarily regulated by hemodynamic factors and is thus increased in rats with chronic hypoxic pulmonary hypertension. Furthermore, we examined the role of endothelin (ET)-1 in this regulatory process, since ET-1 is able to induce eNOS via activation of the ET-B receptor. Therefore, chronic hypoxic rats (10% O2) were treated with the selective ET-A receptor antagonist LU-135252 (50 mg · kg-1 · day-1). Right ventricular systolic pressure and cross-sectional medial vascular wall area of pulmonary arteries rose significantly, and eNOS mRNA levels increased 1.8- and 2.6-fold after 2 and 4 wk of hypoxia, respectively (each P < 0.05). Pulmonary ET-1 mRNA and ET-1 plasma levels increased significantly after 4 wk of hypoxia (each P < 0.05). LU-135252 reduced right ventricular systolic pressure, vascular remodeling, and eNOS gene expression in chronic hypoxic rats (each P < 0.05), whereas ET-1 production was not altered. We conclude that eNOS expression in chronic hypoxic rat lungs is modified predominantly by hemodynamic factors, whereas the ET-B receptor-mediated pathway and hypoxia seem to be less important.

pulmonary hypertension; endothelin; hypoxia; endothelial nitric oxide synthase


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