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(Hypertension. 2006;48:555.)
© 2006 American Heart Association, Inc.
Editorial Commentaries |
From the Hypertension and Vascular Research Division, Henry Ford Hospital, and Department of Physiology, Wayne State University, Detroit, Mich.
Correspondence to William H. Beierwaltes, Henry Ford Health System, 7121 E&R Building, 2799 W Grand Blvd, Detroit, MI 48202. E-mail wbeierw1@hfhs.org
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Carbon monoxide (CO), produced within the body as a product of the catabolism of heme by the enzyme heme oxygenase (HO), has been reported to be a local vasodilator. One of its possible pathways is to stimulate guanylyl cyclase to produce cGMP as a second messenger.1 The parallel to NO, another gaseous signaling molecule that also works through cGMP-mediated pathways (although more potent), is obvious. In fact, the vasodilator actions of these 2 may be integrally linked. Both are endothelium derived.2 NO stimulation of cGMP may facilitate CO-mediated dilation of resistance vessels through calcium-activated potassium channels.3 However, the HOCO story has not received the same interest and attention as NO, nor is it as generally well understood by those who work outside the field. In the present issue, we are presented with a provocative study by one of the well-established laboratories within the field of HOCO. Wang et al4 focus on HO in the genetic model of hypertension, the spontaneously hypertensive rat (SHR). They report that 3 weeks of administration of hemin, the oxidation product of heme, which is both a substrate for and an inducer of HO, produced a profound 80-mmHg decrease in blood pressure that was sustained completely for 9 months after ceasing treatment (a duration in a rats life, which roughly translates into 17.5 human years). Although this is a remarkable, hopeful, and possibly profound observation, the study probably raises more questions than it answers.
First, it is important to point out that this sustained decrease in
Related Article:
Hypertension 2006 48: 685-692.
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