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Issue 1047 coverThe Communicative Cardiac Cell Volume 1047 published June 2005
Ann. N.Y. Acad. Sci. 1047: 183–196 (2005). doi: 10.1196/annals.1341.017
Copyright © 2005 by the New York Academy of Sciences
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Articles by DANSON, E. J.
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Articles by DANSON, E. J.
Articles by PATERSON, D. J.
Cardiac Neurobiology of Nitric Oxide Synthases

EDWARD J. DANSON AND DAVID J. PATERSON

Laboratory of Physiology, University of Oxford, Oxford OX1 3PT, UK

Address for correspondence: E.J.F. Danson, M.D., Ph.D., University Laboratory of Physiology, University of Oxford, Parks Road, Oxford OX1 3PT, UK. Voice: 44 1865 282503; fax: 44 1865 272453. edward.danson{at}physiol.ox.ac.uk

Nitric oxide (NO) is a potent modulator of cardiac and vascular regulation. Its role in cardiac-autonomic neural signaling has received much attention over the last decade because of the ability of NO to alter cardiac sympathovagal balance to favor more anti-arrhythmic states. Complexity and controversy have arisen, however, because of the numerous sources of NO in the brain, peripheral nerves, and cardiomyocytes, all of which are potential regulators of cardiac excitability and calcium signaling. This review addresses the integrative role of NO as a relatively ubiquitous signaling molecule with respect to cardiac neurobiology. The present idea, that divergent NO-signaling pathways from multiple sources within the heart and nervous system converge to modulate cardiac excitability and impact on morbidity and mortality in health and disease, is discussed.

Key Words: autonomic • Ca2+ signaling • heart regulation • nitric oxide






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