Journal of Applied Physiology Ad Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

J Appl Physiol (October 4, 2002). doi:10.1152/japplphysiol.00239.2002
This Article
Right arrow Full Text (PDF) Free
Right arrow All Versions of this Article:
94/2/446    most recent
00239.2002v1
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Blumberg, F. C
Right arrow Articles by Pfeifer, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Blumberg, F. C
Right arrow Articles by Pfeifer, M.

Articles in PresS, published online ahead of print October 4, 2002
J Appl Physiol, 10.1152/jap.00239.2002
Submitted on March 19, 2002
Accepted on September 27, 2002

Effects of ET-A Receptor Blockade on eNOS Gene Expression in Chronic Hypoxic Rat Lungs

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

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

* To whom correspondence should be addressed. E-mail: friedrich.blumberg{at}klinik.uni-regensburg.de.

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 LU135252 (LU, 50 mg/kg/d). Right ventricular systolic pressure (RVSP) and cross-sectional medial vascular wall area of pulmonary arteries rose significantly, and eNOS mRNA levels increased 1.8-fold and 2.6-fold after 2 and 4 weeks of hypoxia, respectively (each p<0.05). Pulmonary ET-1 mRNA and ET-1 plasma levels increased significantly after 4 weeks of hypoxia (each p<0.05). LU reduced RVSP, vascular remodeling and eNOS gene expression in chronic hypoxic rats (each p<0.05), while ET-1 production was not altered. We conclude that eNOS expression in chronic hypoxic rat lungs is modified predominantly by hemodynamic factors, while the ET-B receptor-mediated pathway and hypoxia seem less important.




This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
M. Oka, V. Karoor, N. Homma, T. Nagaoka, E. Sakao, S. M. Golembeski, J. Limbird, M. Imamura, S. A. Gebb, K. A. Fagan, et al.
Dehydroepiandrosterone upregulates soluble guanylate cyclase and inhibits hypoxic pulmonary hypertension
Cardiovasc Res, June 1, 2007; 74(3): 377 - 387.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
S. de Frutos, R. Spangler, D. Alo, and L. V. G. Bosc
NFATc3 Mediates Chronic Hypoxia-induced Pulmonary Arterial Remodeling with {alpha}-Actin Up-regulation
J. Biol. Chem., May 18, 2007; 282(20): 15081 - 15089.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
M. Imamura, B. Luo, J. Limbird, A. Vitello, M. Oka, D. D. Ivy, I. F. McMurtry, C. V. Garat, M. B. Fallon, and E. P. Carter
Hypoxic pulmonary hypertension is prevented in rats with common bile duct ligation
J Appl Physiol, February 1, 2005; 98(2): 739 - 747.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 1966 by the American Physiological Society.