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(Hypertension. 2009;53:456.)
© 2009 American Heart Association, Inc.

Editorial Commentaries

Important Role of NAD(P)H Oxidase 2 in the Regulation of the Tubuloglomerular Feedback

From the Department of Medical Cell Biology (M.C., A.E.G.P.), Division of Integrative Physiology, Uppsala University, Uppsala, Sweden; and the Department of Physiology and Pharmacology (M.C.), Division of Pharmacology, Karolinska Institutet, Stockholm, Sweden.

Correspondence to Mattias Carlström, Department of Medical Cell Biology, Uppsala University, S-751 23 Uppsala, Sweden. E-mail Mattias.Carlstrom@mcb.uu.se

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

The tubuloglomerular feedback (TGF) mechanism is a negative feedback loop that senses changes in luminal NaCl delivery at the macula densa (MD) in the juxtaglomerular apparatus and adjusts the vascular tone of the afferent arteriole accordingly.¹ This mechanism contribute importantly to the kidney’s ability to regulate renal microcirculation, fluid homeostasis, and, consequently, blood pressure. Adenosine appears to be the mediator of TGF,² whereas angiotensin II, NO, and superoxide (O₂^–) have important roles in modulating the response. A decrease in NO in the juxtaglomerular apparatus is associated with increased TGF sensitivity and an increase in arterial blood pressure.

Oxidative stress results from a shift in balance between the production of reactive oxygen species and action of antioxidant systems, in favor of reactive oxygen species, and has been implicated in the pathogenesis of hypertension.³ O₂^– is one of the main reactive oxygen species and is in the kidney predominantly formed by NADPH oxidases (NOXs) in the vasculature, cortex, and medulla. MD cells express the main units of NOX and produce O₂^– in response to angiotensin II or increased NaCl load. O₂^– has been shown to enhance the TGF response primarily by scavenging NO in the MD but also directly by constricting the afferent arteriole.⁴

Five NOX isoforms (NOX1 to 5) with a distinct tissue distribution have been found, and the potential isoforms expressed in the kidney are NOX1, NOX2, and NOX4. Using isolated and perfused afferent arterioles from NOX2-deficient mice, it was demonstrated recently that NOX2 (also known as gp91phox) plays . . . [Full Text of this Article]