Abstract
The present study was designed to evaluate the differences in the coronary vasodilator actions of serotonin (5-HT) in isolated heart obtained from naive or castrated male and female rats that were treated with either estrogen or testosterone. Hearts from 12 groups of rats were used: male and female naive animals, castrated, castrated and treated with 17beta-estradiol (0.5 microg kg(-1) day(-1)) for 7 or 30 days, and castrated and treated with testosterone (0.5 mg kg(-1) day(-1)) for 7 or 30 days. After treatment, the vascular reactivity of the coronary bed was evaluated. Baseline coronary perfusion pressure (CPP) was determined and dose-response curves to 5-HT were generated. Baseline CPP differed between male (70 +/- 6 mmHg, N = 10) and female (115 +/- 6 mmHg, N = 12) naive rats. Maximal 5-HT-induced coronary vasodilation was higher (P<0.05) in naive female than in naive male rats. In both sexes, 5-HT produced endothelium-dependent coronary vasodilation. After castration, there was no significant difference in baseline CPP between hearts obtained from male and female rats (75 +/- 7 mmHg, N = 8, and 83 +/- 5 mmHg, N = 8, respectively). Castration reduced the 5-HT-induced maximal vasodilation in female and male rats (P<0.05). Estrogen treatment of castrated female rats restored (P<0.05) the vascular reactivity. In castrated male rats, 30 days of estrogen treatment increased (P<0.05) the responsiveness to 5-HT. The endothelium-dependent coronary vasodilator actions of 5-HT are greater in female rats and are modulated by estrogen. A knowledge of the mechanism of action of estrogen on coronary arteries could aid in the development of new therapeutic strategies and potentially decrease the incidence of cardiovascular disease in both sexes.
Highlights
Coronary artery disease is an important cause of morbidity and mortality
Treatment of castrated female rats with testosterone for 7 days resulted in a baseline coronary perfusion pressure (CPP) that was not significantly different from control, but treatment with testosterone for 30 days resulted in a significant (P
We found that basal CPP was significantly higher in hearts obtained from naive female rats than in hearts obtained from male rats
Summary
Coronary artery disease is an important cause of morbidity and mortality. The disease involves increased vasoconstrictor responses, enhanced interaction of circulating blood cells with blood vessel walls and proliferation and migration of vascular smooth muscle [1]. These events impair coronary blood flow during exercise and under resting conditions. Several studies have demonstrated that the incidence of cardiovascular diseases is higher in men compared with premenopausal women. This difference exists in agonist-induced vascular responses of experimental animals [2,3,4]. Little is known about the mechanisms underlying this phenomenon, epidemiological and experimental evidence indicates that female sex hormones, in particular 17ß-estradiol, have protective effects against cardiovascular diseases [5,6] because estrogen replacement therapy reduces the incidence of coronary artery disease [7,8]
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