title: Methods in the evaluation of cardiovascular renin angiotensin aldosterone activation and oxidative stress.
abstract: Renin angiotensin aldosterone system (RAAS) activation plays an essential role in the development of cardiovascular disease (CVD). Multiple pathophysiologic processes are able to activate RAAS, among which hypertension, obesity, diabetes mellitus 2, and chronic kidney disease deserve special attention, because they are the main contributors to CVD. Adding to the well-known effects of RAAS overactivity on the vasculature and water and electrolyte balance, current evidence links abnormal activation of the RAAS to increased production of reactive oxygen species (ROS) and oxidative stress. This association is mediated at least partially through interaction of angiotensin II (Ang II) with its receptor angiotensin receptor 1 (AT1R) in cardiovascular tissue, and subsequent activation of the nicotinamide adenine dinucleotide phosphate (NADPH) enzymatic complex, which finally leads to increased ROS production. This resulting state of enhanced oxidative stress contributes largely to generalized atherosclerosis and finally to CVD. The generation of animal models of increased RAAS and Ang II expression, in particular the Ren2 rodent model, provides important opportunities to better characterize the relationship between this system and the production of ROS. This chapter describes methods to evaluate, characterize, and quantify the activity of the RAAS and NADPH oxidase, as well as the production of ROS production in animal model of RAAS.
authors.affiliation: University of Missouri, Harry S. Truman VA Hospital, Columbia, Missouri, USA.
authors.forename: Camila
authors.initials: C
authors.lastname: Manrique
authors.forename: Guido
authors.initials: G
authors.lastname: Lastra
authors.forename: Javad
authors.initials: J
authors.lastname: Habibi
authors.forename: Yongzhong
authors.initials: Y
authors.lastname: Wei
authors.forename: E Matthew
authors.initials: EM
authors.lastname: Morris
authors.forename: Craig S
authors.initials: CS
authors.lastname: Stump
authors.forename: James R
authors.initials: JR
authors.lastname: Sowers
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D004195:Disease Models, Animal; D006352:Heart Ventricles / Q000166:cytology / Q000378:metabolism; D006973:Hypertension / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism*; D019255:NADPH Oxidases / Q000378:metabolism; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D012083:Renin / Q000235:genetics / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000502:physiology*
chemical_list: D017382:Reactive Oxygen Species; D019255:NADPH Oxidases; D012083:Renin