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Am J Physiol Heart Circ Physiol 292: H1237-H1244, 2007. First published December 1, 2006; doi:10.1152/ajpheart.00965.2006 Free Article
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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

Karel Rakusan,1 Zuzana Chvojkova,2,3 Patricia Oliviero,2 Ivana Ostadalova,3 Frantisek Kolar,3 Catherine Chassagne,2 Jane-Lise Samuel,2 and Bohuslav Ostadal3

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{alpha} 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


Address for reprint requests and other correspondence: B. Ostadal, Inst. of Physiology, Academy of Sciences of the Czech Republic, Videnska 1083, 142 20 Prague 4, Czech Republic (e-mail: ostadal{at}biomed.cas.cz)






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