title: Lowering arterial pressure delays the oxidative stress generation in a renal experimental model of hypertension.
abstract: Oxidative stress produced through reactive oxygen species (ROS) enhancement is considered to play a key role in the development and maintenance of hypertension. In the vasculature, the most important source of ROS is the reduced nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase enzyme. The principal stimulus of this enzyme is angiotensin II (Ang II). However, oxidative stress seems to be present in virtually all forms of hypertension including low-renin hypertension, where the levels of Ang II are reduced. For this reason, the question is if ROS generation is induced by Ang II or it is a consequence of hypertension. We used as hypertensive model the aortic coarctated rats, which were treated with losartan or minoxidil for 7 days. Thoracic aortic segments were excised, and the NAD(P)H oxidase subunits expression, oxidative stress parameters, and heme oxygenase-1 abundance were evaluated. Hypertensive animals had an increase in the activity and expression of NAD(P)H oxidase and, as a consequence, in the oxidative stress parameters. Interestingly, either losartan or minoxidil administration blunted those parameters, indicating that arterial pressure is the key factor in the development of oxidative stress in the hypertensive aorta. We suggest that antihypertensive drug administration at the beginning of this pathology delays the oxidative stress generation, thus preventing the aggravation of this disease.
authors.affiliation: Departamento de Química Biológica, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires 1113, Argentina. arielp@qb.ffyb.uba.ar
authors.forename: Ariel H
authors.initials: AH
authors.lastname: Polizio
authors.forename: Susana B
authors.initials: SB
authors.lastname: Gorzalczany
authors.forename: María L
authors.initials: ML
authors.lastname: Tomaro
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D001013:Aorta, Thoracic / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects*; D004195:Disease Models, Animal; D006419:Heme Oxygenase (Decyclizing) / Q000378:metabolism; D006977:Hypertension, Renal / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D019808:Losartan / Q000008:administration & dosage / Q000627:therapeutic use; D008297:Male; D008914:Minoxidil / Q000008:administration & dosage / Q000627:therapeutic use; D019255:NADPH Oxidases / Q000096:biosynthesis; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D000959:Antihypertensive Agents; D017382:Reactive Oxygen Species; D008914:Minoxidil; D006419:Heme Oxygenase (Decyclizing); C491523:Hmox1 protein, rat; D019255:NADPH Oxidases; D019808:Losartan