Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 2000;102:2162-2164

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Finkel, M. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Finkel, M. S.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Medline Plus Health Information
*Cardiomyopathy
Hazardous Substances DB
*NITRIC OXIDE
Related Collections
Right arrow Structure
Right arrow Contractile function
Right arrow Biochemistry and metabolism
Right arrow Congestive
Right arrow Animal models of human disease
Right arrow Apoptosis
Right arrow Calcium cycling/excitation-contraction coupling
Right arrow Cell biology/structural biology
Right arrow Cell signalling/signal transduction
Right arrow Gene expression
Right arrow Gene regulation
Right arrow Growth factors/cytokines
Right arrow Heart failure - basic studies
Right arrow Ischemic biology - basic studies
Right arrow Ion channels/membrane transport
Right arrow Physiological and pathological control of gene expression
Right arrow Genetics of cardiovascular disease
Right arrow Oxidant stress
Right arrow Receptor pharmacology

(Circulation. 2000;102:2162.)
© 2000 American Heart Association, Inc.


Editorial

Nitric Oxide and Viral Cardiomyopathy

Mitchell S. Finkel, MD

From the West Virginia University School of Medicine, WVU Cardiology, Morgantown, WVa, and Louis A. Johnson VA Medical Center, Clarksburg, WVa.

Correspondence to Mitchell S. Finkel, MD, Department of Medicine, West Virginia University School of Medicine, Medical Center Dr, PO Box 9157, Morgantown, WV 26506-9157. E-mail mfinkel@wvu.edu


Key Words: Editorials • heart failure • ischemia • infection

The report by Badorff et al1 in this issue of Circulation provides an opportunity to reflect on the enormous impact that the discovery of nitric oxide (NO) has already had in furthering our understanding of the basic biology of human disease processes. This report also helps to illustrate how basic insights coupled with clinical observations will ultimately lead to redefining previously unrelated clinical conditions along more pathophysiologically relevant lines.

The 1998 Nobel Prize for Medicine or Physiology was awarded to Louis J. Ignarro, Ferid Murad, and Robert Furchgott for the discovery of the role of NO as a signaling molecule in the cardiovascular system.2 Ignarro studied the mechanism of action of nitroglycerin, which was first synthesized by Sobrero more than 150 years ago, and discovered that it mediates its effects through NO. Murad discovered that NO mediates effects through that "other," less appreciated (ie, not cAMP), cyclic nucleotide, cGMP. Furchgott’s simple experiments with rabbit aortas provided physiological relevance by revealing that vascular endothelium normally produces a relaxing factor, endothelium-derived relaxing factor, which Ignarro showed to be NO. Shortly thereafter, inhibitors were identified, enzyme proteins isolated, and NO synthases (NOS) successively cloned from neurons (type 1), macrophages (type 2), and endothelial cells (type 3).3 It was clear from the beginning that the constitutive, basal production of small quantities of NO by NOS types 1 and 3 played a critical role in normal physiological processes. What has been less obvious, however, is the benefits conferred by the production of much larger quantities . . . [Full Text of this Article]