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Cardiovascular Research 2005 67(4):575-577; doi:10.1016/j.cardiores.2005.06.018
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Copyright © 2005, European Society of Cardiology

Increased eNOS expression as a compensatory mechanism reducing β-adrenergic responsiveness?

Frank U. Müller

Institute of Pharmacology and Toxicology, University of Münster, Domagkstrasse 12, D-48149 Münster, Germany

Received 16 June 2005; accepted 21 June 2005

The first 10% of the full text of this article appears below.

See article by Danson et al. [13] (pages 613–623) in this issue.

Nitric oxide (NO) is an important regulatory factor of the cardiovascular system mediating endothelium-dependent vasodilatation and modulating different facets of cardiac function including heart rate, contraction, relaxation, cell growth, and survival [1–3]. NO is synthesized from L-arginine by NO synthases (NOS), a family of isoenzymes with characteristic functional and regulatory properties [4]. All three NOS isoforms, i.e. the neural isoform (nNOS), the inducible isoform (iNOS, induced upon stimulation with appropriate inflammatory mediators), and the endothelial isoform (eNOS), can be expressed within various cell types in cardiac muscle. In the heart, eNOS was identified in endocardial and endothelial cells, in cardiomyocytes, and in specialized cells of . . . [Full Text of this Article]


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