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Updated: Jun 2, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
Published on: June 7, 2016
Angiotensin II induced catabolic effect and muscle atrophy are redox dependent
Laura C Semprun-Prieto1, Sergiy Sukhanov, Tadashi Yoshida
1Heart 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.
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 p47(phox)(-/-) mice with vehicle or Ang II for 7days. Superoxide production was increased 2.4-fold in the skeletal muscle of Ang II infused mice, and this increase was prevented in p47(phox)(-/-) 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 p47(phox)(-/-) 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 p47(phox)(-/-) mice. In conclusion, Ang II-induced skeletal muscle wasting is in part dependent on NADPH oxidase derived ROS.
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