Document Detail

Role of nitric oxide in the pathophysiology of heart failure.
MedLine Citation:
PMID:  12652158     Owner:  NLM     Status:  MEDLINE    
Nitric oxide (NO) plays critical roles in the regulation of integrated cardiac and vascular function and homeostasis. An understanding of the physiologic role and relative contribution of the three NO synthase isoforms (neuronal--NOS1, inducible--NOS2, and endothelial--NOS3) is imperative to comprehend derangements of the NO signaling pathway in the failing cardiovascular system. Several theories of NO and its regulation have developed as explanations for the divergent observations from studies in health and disease states. Here we review the physiologic and pathophysiologic influence of NO on cardiac function, in a framework that considers several theories of altered NO signaling in heart failure. We discuss the notion of spatial compartmentalization of NO signaling within the myocyte in an effort to reconcile many controversies about derangements in the influences of NO in the heart and vasculature.
Hunter C Champion; Michel W Skaf; Joshua M Hare
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Heart failure reviews     Volume:  8     ISSN:  1382-4147     ISO Abbreviation:  Heart Fail Rev     Publication Date:  2003 Jan 
Date Detail:
Created Date:  2003-03-24     Completed Date:  2003-06-27     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9612481     Medline TA:  Heart Fail Rev     Country:  United States    
Other Details:
Languages:  eng     Pagination:  35-46     Citation Subset:  IM    
Division of Cardiology, Department of Medicine, Johns Hopkins Hospital, Baltimore, MD 21287, USA.
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MeSH Terms
Endothelium, Vascular / cytology,  metabolism,  physiopathology
Heart Failure / physiopathology*
Myocytes, Cardiac / metabolism
Nitric Oxide / physiology*
Signal Transduction / physiology
Grant Support
Reg. No./Substance:
10102-43-9/Nitric Oxide

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