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Reactive oxygen species as important determinants of medullary flow, sodium excretion, and hypertension. Am J Physiol Renal Physiol 2015 Feb 01;308(3):F179-97

Date

10/31/2014

Pubmed ID

25354941

Pubmed Central ID

PMC4312962

DOI

10.1152/ajprenal.00455.2014

Scopus ID

2-s2.0-84922264751 (requires institutional sign-in at Scopus site)   89 Citations

Abstract

The physiological evidence linking the production of superoxide, hydrogen peroxide, and nitric oxide in the renal medullary thick ascending limb of Henle (mTAL) to regulation of medullary blood flow, sodium homeostasis, and long-term control of blood pressure is summarized in this review. Data obtained largely from rats indicate that experimentally induced elevations of either superoxide or hydrogen peroxide in the renal medulla result in reduction of medullary blood flow, enhanced Na(+) reabsorption, and hypertension. A shift in the redox balance between nitric oxide and reactive oxygen species (ROS) is found to occur naturally in the Dahl salt-sensitive (SS) rat model, where selective reduction of ROS production in the renal medulla reduces salt-induced hypertension. Excess medullary production of ROS in SS rats emanates from the medullary thick ascending limbs of Henle [from both the mitochondria and membrane NAD(P)H oxidases] in response to increased delivery and reabsorption of excess sodium and water. There is evidence that ROS and perhaps other mediators such as ATP diffuse from the mTAL to surrounding vasa recta capillaries, resulting in medullary ischemia, which thereby contributes to hypertension.

Author List

Cowley AW Jr, Abe M, Mori T, O'Connor PM, Ohsaki Y, Zheleznova NN

Author

Allen W. Cowley Jr PhD Professor in the Physiology department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Humans
Hypotension
Kidney Medulla
NADPH Oxidases
Nitric Oxide
Reactive Oxygen Species
Sodium