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(Hypertension. 2005;45:847.)
© 2005 American Heart Association, Inc.

Editorial Commentaries

Triggering Mitochondrial Radical Release

A New Function for NADPH Oxidases

Ralf P. Brandes

From the Institut für Kardiovaskuläre Physiologie Fachbereich Medizin J.W. Goethe-Universität, Frankfurt am Main Germany.

Correspondence to Ralf P. Brandes, MD, Institut für Kardiovaskuläre Physiologie Fachbereich Medizin J.W. Goethe-Universität Theodor-Stern-Kai 7 D-60596 Frankfurt am Main Germany. E-mail r.brandes@em.uni-frankfurt.de

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

Ischemic preconditioning describes a scenario in which brief intermittent periods of ischemia provide protection against subsequent ischemic injury.¹ A number of elements in the signal transduction cascade mediating ischemic preconditioning have been identified. The opening of mitochondrial K_ATP channels is central for this process, as well as the subsequent release of reactive oxygen species (ROS) from mitochondria, and finally the activation of p38 mitogen–activated protein kinase (p38 MAP kinase). In addition to intermittent ischemia, several agonists, such as acetylcholine, phenylephrine, bradykinin, and opioids have been demonstrated to elicit (pharmacological) preconditioning² by a similar pathway.

In this issue of Hypertension, Kimura et al extend this list of preconditioning agents by including angiotensin II.³ In particular, they demonstrate that angiotensin II leads to the assembly of the NADPH oxidase in the rat myocardium and that inhibition of this assembly process using apocynin blocks angiotensin II–mediated preconditioning. Moreover, the authors observed that inhibition of mitochondrial K_ATP channels by 5-hydroxydecanoate (5-HD) blocked not only the preconditioning effect of angiotensin II but also prevented the angiotensin II–induced ROS formation from cardiac myocytes. 5-HD had no antioxidative properties and did not block the respiratory burst in leukocytes but prevented ROS formation of isolated mitochondrial preparations. Therefore, the authors conclude that the effects observed in response to angiotensin II in rat myocardium, such as lipid peroxidation, p38 MAP kinase activation, and preconditioning, are mediated by mitochondrial ROS (Figure).

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Role of NAD(P)H Oxidase- and Mitochondria-Derived Reactive Oxygen Species in Cardioprotection of Ischemic Reperfusion Injury by Angiotensin II

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Hypertension 2005 45: 860-866. [Abstract] [Full Text] [PDF]

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