HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

Am J Physiol Heart Circ Physiol 292: H1237-H1244, 2007. First published December 1, 2006; doi:10.1152/ajpheart.00965.2006
0363-6135/07 $8.00

This Article Free upon publication Full Text Full Text (PDF) All Versions of this Article: 292/3/H1237    most recent 00965.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Rakusan, K. Articles by Ostadal, B. Search for Related Content PubMed PubMed Citation Articles by Rakusan, K. Articles by Ostadal, B.

CALL FOR PAPERS
Oxygen Sensing: Life and Death of a Cell

ANG II type 1 receptor antagonist irbesartan inhibits coronary angiogenesis stimulated by chronic intermittent hypoxia in neonatal rats

¹Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Canada; ²Institut National de la Santé et de la Recherche Médicale Unité 572, Institut Fédératif de Recherche Jules Marrey, Paris, France; and ³Institute of Physiology, Academy of Sciences of the Czech Republic and Centre for Cardiovascular Research, Prague, Czech Republic

Submitted 6 September 2006 ; accepted in final form 27 November 2006

Chronic hypoxia has been shown to stimulate myocardial microvascular growth and improve cardiac ischemic tolerance in young and adult rats. The aim of this study was to determine whether the ANG II type 1 receptor (AT₁) pathway was involved in these processes. Newborn Wistar rats, exposed to chronic intermittent hypoxia (8 h/day) for 10 days, were simultaneously treated with AT₁ receptor blocker irbesartan and compared with untreated animals. The major finding is that chronic hypoxia increased the capillary supply of myocardial tissue, which was even more pronounced in hypertrophied right ventricle, whereas increased arteriolar supply was found only in the left ventricle. This angiogenic response was completely prevented by irbesartan. Moreover, chronic hypoxia improved the postischemic recovery of cardiac contractile function during reperfusion, and this protective effect was also completely abolished by irbesartan. Chronic hypoxia increased the myocardial density of AT₁ but not of ANG II type 2 receptor subtypes, whereas the effect of irbesartan was not significant. The expression of caveolin-1 markedly increased in response to chronic hypoxia, and irbesartan prevented this effect. Neither hypoxia nor irbesartan treatment altered the expression of nitric oxide synthase 3, heat shock protein 90, and VEGF. It is concluded that the AT₁ receptor pathway plays an important role in coronary angiogenesis and improved cardiac ischemic tolerance induced in neonatal rats by chronic hypoxia.

angiotensin II receptors; ischemia-reperfusion; caveolin-1

This article has been cited by other articles:

				L. P. Christensen, R.-l. Zhang, W. Zheng, J. J. Campanelli, E. I. Dedkov, R. M. Weiss, and R. J. Tomanek Postmyocardial infarction remodeling and coronary reserve: effects of ivabradine and beta blockade therapy Am J Physiol Heart Circ Physiol, July 1, 2009; 297(1): H322 - H330. [Abstract] [Full Text] [PDF]