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Hypertension. 2006;48:552-554
Published online before print August 28, 2006, doi: 10.1161/01.HYP.0000238142.22799.80
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(Hypertension. 2006;48:552.)
© 2006 American Heart Association, Inc.


Editorial Commentaries

NO and Central Cardiovascular Control

A Simple Molecule With a Complex Story

William T. Talman

From the Department of Neurology, Carver College of Medicine University of Iowa, Veterans Affairs Medical Center, Iowa City.

Correspondence to Department of Neurology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242. E-mail william-talman@uiowa.edu


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

The 1998 Nobel Prize in Physiology or Medicine recognized the great contributions of Robert Furchgott, Louis Ignarro, and Ferid Murad through "their discoveries concerning nitric oxide as a signaling molecule in the cardiovascular system." Furchgott’s earlier work describing a vasodilatory factor that was activated by acetylcholine acting on an intact endothelium not only set the stage for subsequent recognition that NO was the endothelium-derived relaxation factor but also acted as a harbinger of much subsequent study of interactions between classic neurotransmitters and NO. Three isoforms of NO synthase (NOS), the biosynthetic enzyme for synthesis of NO, have been identified. Two are constitutive enzymes, endothelial NOS (eNOS) and neuronal NO (nNOS). Each has been identified in the nucleus tractus solitarii (NTS), the primary site of termination of baroreceptor afferent nerves, but the role of each, or for that matter the role of NO itself, in baroreflex transmission through the NTS remains very much in question. The presence of iNOS in the NTS could indicate that there had been stress in animals in which it was found.

In keeping with the potential that NO may link transmitter mechanisms and may integrate vascular and neuronal functions, the work by Waki et al in this issue of Hypertension1 provides further evidence for complex integration through NO mechanisms in the NTS and for contributions of NO in disorders of cardiovascular homeostasis. That work is the latest from the Paton/Kasparov laboratories at the University of Bristol and further supports there being a cascade of transduction events . . . [Full Text of this Article]


Related Article:

Endothelial NO Synthase Activity in Nucleus Tractus Solitarii Contributes to Hypertension in Spontaneously Hypertensive Rats
Hidefumi Waki, David Murphy, Song T. Yao, Sergey Kasparov, and Julian F.R. Paton
Hypertension 2006 48: 644-650. [Abstract] [Full Text] [PDF]