Published online before print September 21, 2009, doi: 10.1161/HYPERTENSIONAHA.109.137984
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(Hypertension. 2009;54:964.)
© 2009 American Heart Association, Inc.
Editorial Commentaries |
A New PIXel in the Puzzle
How Increased Vascular Pressure Induces Oxidative Stress
Correspondence to Ralf P. Brandes, Institut für Kardiovaskuläre Physiologie, Johann Wolfgang Goethe-Universität, Theodor-Stern-Kai 7, D-60596 Frankfurt am Main, Germany. E-mail r.brandes@em.unifrankfurt.de
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Hypertension is a clinical situation associated with endothelial dysfunction and increased vascular reactive oxygen species (ROS) formation. The observations that antioxidants, such as Tempol or apocynin, lower the blood pressure in spontaneously hypertensive rats gave rise to the concept that ROS essentially contribute to hypertension. Recent work, however, has sharpened this view, and it is now clear that the underlying mechanism of ROS-induced hypertension may not be endothelial dysfunction but rather an ROS-dependent modulation of the sympathetic drive,1 the kidney, and potentially alterations in the immune system.2 Despite these findings, hypertension has been consistently linked to increased ROS formation in the vascular system. It is, therefore, plausible that ROS are not necessarily the cause but potentially the consequence of hypertension. This notion certainly does not exclude that ROS are involved in the pathogenesis of specific aspects of hypertension, such as the development of fibrosis.
In keeping with the concept of hypertension-induced ROS formation, it was noted previously that distension of a vessel with an oversized balloon acutely increases ROS formation.3 Moreover, acute elevation of pressure from 80 to 160 mm Hg enhances the ROS formation and induces an ROS-dependent attenuation of the endothelium-dependent relaxation in isolated rat femoral arteries.4 Moreover, even in chronic models of isolated hypertension, such as aortic banding, the ROS formation was consistently higher in the hypertensive rather than in the normotensive part.
There is, however, uncertainty regarding the enzymatic sources of ROS, and a contribution of mitochondria, endothelial NO synthase uncoupling, and NADPH oxidases has been
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