Influence of ovariectomy on cardiac oxidative stress in a renovascular hypertension model

• Published in: Canadian journal of physiology and pharmacology Vol. 90; no. 9; p. 1229
• Main Authors: Barp, Jaqueline, Sartório, Carmem Luiza, Campos, Cristina, Llesuy, Susana Francisca, Araujo, Alex Sander, Belló-Klein, Adriane
• Format: Journal Article
• Language: English
• Published: Canada 01-09-2012
• Subjects: Animals; Blood Pressure; Catalase - metabolism; Disease Models, Animal; Estrogens - metabolism; Female; Glutathione Peroxidase - metabolism; Hypertension, Renovascular - metabolism; Lipid Peroxidation; Myocardium - enzymology; Myocardium - metabolism; Ovariectomy; Oxidative Stress; Rats; Rats, Wistar; Superoxide Dismutase - metabolism; Thiobarbituric Acid Reactive Substances - metabolism
• ISSN: 1205-7541
• DOI: 10.1139/y2012-078

The aim of this study was to evaluate the potential influence of endogenous ovarian hormones on cardiac oxidative stress in renovascular hypertension. Female Wistar rats (N = 10 per group) were divided among 4 groups: (i) normotensive control; (ii) hypertensive control; (iii) normotensive ovariectomized; and (iv) hypertensive ovariectomized rats. To induce hypertension, 2-kidney 1-clip (2K1C) Goldblatt's method was followed. Blood pressure (BP) was enhanced (25%) in 2K1C and it was not further altered in hypertensive ovariectomized animals. Lipid peroxidation (measured by thiobarbituric acid reactive substances; TBARS) increased in heart homogenates after ovariectomy (253%) and was additionally augmented when associated with hypertension (by 28%). Superoxide dismutase and catalase activities were similar in both hypertensive groups. Hypertension enhanced glutathione peroxidase activity (75%), but the association with ovariectomy prevented this change. Total radical trapping antioxidant potential (TRAP) decreased in hypertensive rats (34%) and was recovered when associated with ovariectomy. However, this adaptation seems not to be sufficient to avoid the increased oxidative damage in ovariectomized hypertensive animals. These results suggest a protective role for physiological ovarian hormones in the cardiac oxidative stress induced by 2K1C hypertension.