title: Is cardiac hypertrophy in spontaneously hypertensive rats the cause or the consequence of oxidative stress?
abstract: The aim of this work was to assess the possible correlation between oxidative damage and the development of cardiac hypertrophy in heart tissue from young (40-d-old) and older (4-, 11- and 19-month-old) spontaneously hypertensive rats (SHR) in comparison with age-matched Wistar (W) rats. To this end, levels of thiobarbituric acid reactive substances (TBARS), nitrotyrosine contents, NAD(P)H oxidase activity, superoxide production, and the activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were determined. Compared to age-matched normotensive rats, SHR showed a significant increase in systolic blood pressure from 40 d of age and left ventricular hypertrophy (LVH) was significantly evident from 4 months of age. W rats (11- and 19-month-old) also showed an increase in LVH with aging. TBARS and nitrotyrosine levels were similar in young rats from both strains and were significantly increased with age in both strains, with the values in SHR being significantly higher than those in age-matched W rats. NAD(P)H activity was similar in young SHR and W rats, whereas it was higher in aged SHR compared with age-matched W rats. Compared to W rats, superoxide production was higher in aged SHR, and was abolished by NAD(P)H inhibition with apocynin. CAT activity was increased in the hearts of 4-month-old SHR compared to age-matched W rats and was decreased in the hearts of the oldest SHR compared to the oldest W rats. SOD and GPx activities decreased in both rat strains with aging. Moreover, an increase in collagen deposition with aging was evident in both rat strains. Taken together, these data showed that aged SHR exhibited higher cardiac hypertrophy and oxidative damage compared to W rats, indicating that the two undesirable effects are associated. That is, oxidative stress appears to be a cause and/or consequence of hypertrophy development in this animal model.
authors.affiliation: Center of Cardiovascular Research, National University of La Plata, Buenos Aires, Argentina.
authors.forename: María Cecilia
authors.initials: MC
authors.lastname: Alvarez
authors.forename: Claudia
authors.initials: C
authors.lastname: Caldiz
authors.forename: Juliana C
authors.initials: JC
authors.lastname: Fantinelli
authors.forename: Carolina D
authors.initials: CD
authors.lastname: Garciarena
authors.forename: Gloria M
authors.initials: GM
authors.lastname: Console
authors.forename: Gladys E
authors.initials: GE
authors.lastname: Chiappe de Cingolani
authors.forename: Susana M
authors.initials: SM
authors.lastname: Mosca
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000209:etiology / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D003094:Collagen / Q000032:analysis; D005979:Glutathione Peroxidase / Q000378:metabolism; D015227:Lipid Peroxidation; D008297:Male; D019255:NADPH Oxidases / Q000378:metabolism; D018384:Oxidative Stress; D051381:Rats; D011918:Rats, Inbred SHR; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism
chemical_list: D013481:Superoxides; D003094:Collagen; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D019255:NADPH Oxidases