CENTRO DE INVESTIGACIONES CARDIOVASCULARES "DR. HORACIO EUGENIO CINGOLANI"
Unidad Ejecutora - UE
Is cardiac hypertrophy from Spontaneously Hypertensive Rats the cause or the consecuence of oxidative stress?
ÁLVAREZ MC; CALDIZ CI; FANTINELLI JC; GARCIARENA CD; CONSOLE GM; CHIAPPE DE CINGOLANI GE; MOSCA SM
The Japanese Society of Hypertension
Año: 2008 vol. 31 p. 1465 - 1476
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-day-old) and older (4-, 11- and 19-month-old) spontaneously hypertensive rats (SHR) in comparison with age-matched Wistar (W) rats. TBARS and nitrotyrosine contents, NAD(P)H oxidase activity and superoxide production as well as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) antioxidant enzymes activities were determined. Compared to age-matched normotensive rats, SHR showed a significant increase in systolic blood pressure from 40-day-old and left ventricular hypertrophy (LVH) was significantly evident from 4-month-old. 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 but they were significantly increased with aging having SHR higher values than 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. Compared to W rats superoxide production was higher in aged SHR, which was abolished by NAD(P)H inhibition with apocynin. CAT activity increased in hearts of 4-month-old SHR compared to age-matched W rats and decreased in the oldest ones. 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. The overall data show that aged SHR exhibited higher cardiac hypertrophy and oxidative damage compared to W rats, indicating that both undesirable effects are associated. Thus, oxidative stress would be the cause and/or the consequence of hypertrophy development.