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Resveratrol reverses estrogen‐induced hypertension in female rats
Author(s) -
Subramanian Madhan,
Garver Hannah,
Fink Gregory D.,
Mohankumar Sheba,
Mohankumar P. S.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.933.1
Subject(s) - resveratrol , estrogen , medicine , endocrinology , oxidative stress , blood pressure , osteoporosis , hormone , pharmacology
Estrogens used in hormone replacement therapy (HRT) are believed to protect against osteoporosis, memory loss, etc. However, recent evidence indicates that HRT increases the risk of coronary heart disease and stroke. Studies from our laboratory suggest that chronic estrogen exposure causes oxidative stress. Since oxidative stress is known to play an important role in the development of hypertension, we wanted to study if chronic exposure to low levels of estrogen causes hypertension in rats. An antioxidant, resveratrol was used to block the effect of estrogen exposure. Adult female Sprague‐Dawley rats were either sham implanted or implanted (s.c.) with 90‐day slow release estradiol‐17 β (E2; 20 ng/day) pellets. Seven weeks later, they were further divided into two groups and fed chow or chow that contained 0.84g resveratrol/kg. Three weeks later, rats were implanted with telemeters via the femoral artery to monitor blood pressure. E2 exposure increased both mean systolic (MSP) and diastolic pressures (MDP) (mm of Hg; mean ± S.E.) significantly to 134.4± 0.4 and 92.8± 0.2 respectively, compared to control rats (124.1±0.5 and 84.8± 0.3 respectively) (p<0.05). While treatment with resveratrol alone did not alter MSP (122.7±0.4) or MDP (85.1±0.2), it was capable of reversing the increase in both MSP (126.5±0.3) and MDP (84.6± 0.2) caused by E2 exposure (p<0.05). These results indicate that chronic exposure to low levels of E2 can increase blood pressure in female rats and this effect is most probably mediated through oxidative stress pathways. Supported by NIH AG 027697.