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

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal 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 Google Scholar Google Scholar Articles by Grilli, A. Articles by Felaco, M. Search for Related Content PubMed PubMed Citation Articles by Grilli, A. Articles by Felaco, M.

Inducible Nitric Oxide Synthase and Heme Oxygenase-1 in Rat Heart: Direct Effect of Chronic Exposure to Hypoxia

Address correspondence to Professor Mario Felaco, Department of Biomorphology, Faculty of Medicine and Surgery, University G. d’Annunzio, via dei Vestini, Chieti 66013, Italy; tel 39 087 135 55306; fax 39 087 157 4 361; e-mail mfelaco{at}unich.it.

Hypoxia is a potent regulator of various biological process. Mammalian cells respond to hypoxia by increased expression of several genes. The aim of this study was to evaluate the effects of chronic exposure to low oxygen tension on the induction of inducible nitric oxide synthase (iNOS) and heme oxygenase-1 (HO-1) in rat heart. Male Wistar rats were assigned randomly to 4 groups: (A) control rats maintained in normoxic conditions for 7 and 14 days; (B) rats maintained in hypoxic conditions for 7 and 14 days; (C) rats maintained in normoxic conditions for 7 days and then transferred to hypoxic conditions for 7 days; and (D) rats maintained in hypoxic conditions for 7 days and then transferred to normoxic conditions for 7 days. In Group A, iNOS and HO-1 immunoreactivities were not evident; in Group B these immunoreactivities increased from day 7 to 14; in Group C the immunoreactivities decreased on day 7, compared to day 14; and in Group D, the immunoreactivities increased on day 7, compared to day 14. These findings were confirmed by Western blot analyses of the respective proteins and by rt-PCR assays of the corresponding mRNAs. The results indicate that the adaptive response to hypoxia involves up-regulation of HO-1 through iNOS activation in cardiac cells. HO-1 helps to regulate vascular tone via CO and thereby participates in an important cardiac defense mechanism.

Keywords: nitric oxide synthase, heme oxygenase, hypoxia, oxidative stress, rat heart, carbon monoxide

This article has been cited by other articles:

				J. Sunderram, J. Semmlow, S. Thakker-Varia, M. Bhaumik, O. Hoang-Le, and J. A. Neubauer Heme oxygenase-1-dependent central cardiorespiratory adaptations to chronic hypoxia in mice Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2009; 297(2): R300 - R312. [Abstract] [Full Text] [PDF]

				J. L. Scragg, M. L. Dallas, J. A. Wilkinson, G. Varadi, and C. Peers Carbon Monoxide Inhibits L-type Ca2+ Channels via Redox Modulation of Key Cysteine Residues by Mitochondrial Reactive Oxygen Species J. Biol. Chem., September 5, 2008; 283(36): 24412 - 24419. [Abstract] [Full Text] [PDF]

				L. Wu and R. Wang Carbon Monoxide: Endogenous Production, Physiological Functions, and Pharmacological Applications Pharmacol. Rev., December 1, 2005; 57(4): 585 - 630. [Abstract] [Full Text] [PDF]

				B. M. Tsai, M. Wang, M. Clauss, P. Sun, and D. R. Meldrum Endothelial monocyte-activating polypeptide II causes NOS-dependent pulmonary artery vasodilation: a novel effect for a proinflammatory cytokine Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2004; 287(4): R767 - R771. [Abstract] [Full Text] [PDF]