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Am J Physiol Heart Circ Physiol 293: H2009-H2023, 2007. First published June 22, 2007; doi:10.1152/ajpheart.00522.2007
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INVITED REVIEW

Renin-angiotensin-aldosterone system and oxidative stress in cardiovascular insulin resistance

Shawna A. Cooper,1,3 Adam Whaley-Connell,1,3 Javad Habibi,1,3,4 Yongzhong Wei,1,3 Guido Lastra,1 Camila Manrique,1 Sameer Stas,1 and James R. Sowers1,2,3,4

Departments of 1Internal Medicine and 2Medical Pharmacology and Physiology and 3Diabetes and Cardiovascular Center of Excellence, University of Missouri School of Medicine, and 4Harry S. Truman Veterans Affairs Medical Center, Columbia, Missouri

Hypertension commonly occurs in conjunction with insulin resistance and other components of the cardiometabolic syndrome. Insulin resistance plays a significant role in the relationship between hypertension, Type 2 diabetes mellitus, chronic kidney disease, and cardiovascular disease. There is accumulating evidence that insulin resistance occurs in cardiovascular and renal tissue as well as in classical metabolic tissues (i.e., skeletal muscle, liver, and adipose tissue). Activation of the renin-angiotensin-aldosterone system and subsequent elevations in angiotensin II and aldosterone, as seen in cardiometabolic syndrome, contribute to altered insulin/IGF-1 signaling pathways and reactive oxygen species formation to induce endothelial dysfunction and cardiovascular disease. This review examines currently understood mechanisms underlying the development of resistance to the metabolic actions of insulin in cardiovascular as well as skeletal muscle tissue.


Address for reprint requests and other correspondence: J. R. Sowers, Director of the Missouri Univ. Diabetes and Cardiovascular Center, D109 HSC Diabetes Center, One Hospital Dr., Columbia, MO 65212 (e-mail: sowersj{at}health.missouri.edu)




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