Angiotensin II induced catabolic effect and muscle atrophy are redox dependent |
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| Authors: | Semprun-Prieto Laura C Sukhanov Sergiy Yoshida Tadashi Rezk Bashir M Gonzalez-Villalobos Romer A Vaughn Charlotte Michael Tabony A Delafontaine Patrice |
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| Affiliation: | aHeart and Vascular Institute, Tulane University School of Medicine, Tulane University Heart and Vascular Institute, 1430 Tulane Avenue, SL 48, New Orleans, LA 70112, United States;bDepartment of Physiology, Tulane University School of Medicine, 1430 Tulane Avenue, SL 48, New Orleans, LA 70112, United States;cHypertension and Renal Center of Excellence, Tulane University School of Medicine, 1430 Tulane Avenue, SL 48, New Orleans, LA 70112, United States |
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| Abstract: | ![]()
Angiotensin II (Ang II) causes skeletal muscle wasting via an increase in muscle catabolism. To determine whether the wasting effects of Ang II were related to its ability to increase NADPH oxidase-derived reactive oxygen species (ROS) we infused wild-type C57BL/6J or p47phox−/− mice with vehicle or Ang II for 7 days. Superoxide production was increased 2.4-fold in the skeletal muscle of Ang II infused mice, and this increase was prevented in p47phox−/− mice. Apocynin treatment prevented Ang II-induced superoxide production in skeletal muscle, consistent with Ang II increasing NADPH oxidase derived ROS. Ang II induced loss of body and skeletal muscle weight in C57BL/6J mice, whereas the reduction was significantly attenuated in p47phox−/− animals. The reduction of skeletal muscle weight caused by Ang II was associated with an increase of proteasome activity, and this increase was completely prevented in the skeletal muscle of p47phox−/− mice. In conclusion, Ang II-induced skeletal muscle wasting is in part dependent on NADPH oxidase derived ROS. |
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| Keywords: | Abbreviations: Ang II, angiotensin II DHE, dihydroethidium ROS, reactive oxygen species NADPH, nicotinamide adenine dinucleotide phosphate |
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