AJP - Heart Calcium Transients and Cell-Sarcomere
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol (February 28, 2002). doi:10.1152/ajpheart.00817.2001
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
283/1/H69    most recent
00817.2001v1
Right arrow Alert me when this article is cited
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 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 Csont, T.
Right arrow Articles by Ferdinandy, P.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Csont, T.
Right arrow Articles by Ferdinandy, P.

Articles in PresS, published online ahead of print February 28, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00817.2001
Submitted on September 17, 2001
Accepted on February 26, 2002

Nitrate tolerance does not increase production of peroxynitrite in the heart

Tamas Csont1, Csaba Csonka1, Annamaria Onody1, Aniko Gorbe1, Laszlo Dux1, Richard Schulz2, Gary F Baxter3, and Peter Ferdinandy1*

1 Biochemistry, University of Szeged, Szeged, Hungary
2 Pharmacology and Pediatrics, University of Alberta, Edmonton, Alberta, Canada
3 The Royal Veterinary College, University of London, London, United Kingdom

* To whom correspondence should be addressed. E-mail: peter{at}biochem.szote.u-szeged.hu.

Clinical studies suggested that long-term nitrate treatment does not improve and may even worsen cardiovascular mortality, and the possible role of nitrate tolerance was suspected. Nitrate tolerance has been recently shown to increase vascular superoxide and peroxynitrite production leading to vascular dysfunction. Nevertheless, nitrates exert direct cardiac effects independent from their vascular actions. Therefore, here we investigated whether in vivo nitroglycerin treatment leading to vascular nitrate tolerance increases cardiac formation of nitric oxide (NO), reactive oxygen species, and peroxynitrite thereby leading to cardiac dysfunction. Nitrate tolerance increased bioavailability of NO in the heart without increasing formation of reactive oxygen species. Despite elevated myocardial NO, neither cardiac markers of peroxynitrite formation, nor cardiac mechanical function were affected by nitroglycerin treatment. However, serum free nitrotyrosine, a marker for systemic peroxynitrite formation, was significantly elevated in nitroglycerin-treated animals. This is the first demonstration that although the systemic effects of nitroglycerin may be deleterious due to enhancement of extracardiac peroxynitrite formation, nitroglycerin does not result in oxidative damage in the heart.




This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
T. Csont, E. Bereczki, P. Bencsik, G. Fodor, A. Gorbe, A. Zvara, C. Csonka, L. G. Puskas, M. Santha, and P. Ferdinandy
Hypercholesterolemia increases myocardial oxidative and nitrosative stress thereby leading to cardiac dysfunction in apoB-100 transgenic mice
Cardiovasc Res, October 1, 2007; 76(1): 100 - 109.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
R. Parent, N. Leblanc, and M. Lavallee
Nitroglycerin reduces myocardial oxygen consumption during exercise despite vascular tolerance
Am J Physiol Heart Circ Physiol, March 1, 2006; 290(3): H1226 - H1234.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 1976 by the American Physiological Society.