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Abstract

Menopause is accompanied by a dramatic increase in incident hypertension, suggesting a protective effect of estrogen on blood pressure. Although estrogen has been shown to decrease sympathetic nerve activity (SNA) and blood pressure (BP) in ovariectomized rats, SNA has not been recorded during estrogen replacement therapy (ERT) in humans. Therefore, the purpose of the study is to determine if chronic ERT causes a sustained decrease in SNA and BP. In 12 normotensive postmenopausal women, we measured 24-hour ambulatory BP and SNA before and after eight weeks of transdermal estradiol (200 mcg/day), oral conjugated estrogens (0.625 mg/day), or placebo, using a randomized crossover design. The major new finding was that transdermal ERT decreased SNA by 30% (from 40 +/- 4 to 27 +/- 4 bursts/min, p = 0.0001) and ambulatory diastolic BP by 5 +/- 2 mmHg (p = 0.0003), whereas, in the same women, oral ERT was without effect. Because the liver is exposed to supraphysiological concentration of estrogen during oral ERT, we speculate that adverse first-pass hepatic effects of estrogen trigger secondary sympathoexcitation and negate primary inhibitory effect of estrogen. Therefore, we measured serum insulin-like growth factor I (IGF-I), a sympathoinhibitory peptide which is produced in the liver but decreased after menopause. We found that serum IGF-I decreased only with oral ERT (from 148+/-12 to 114 +/-9 ng/ml) but was unaffected by transdermal ERT or placebo. In conclusion, transdermal ERT decreases SNA and causes a small but statistically significant decrease in ambulatory blood pressure in normotensive postmenopausal women. Sympathetic inhibition is evident only with transdermal rather than oral ERT whereas the circulating IGF-I is reduced only with oral but not transdermal ERT. These data provide support for the hypothesis that estrogen exerts direct effect on the central nervous system to decrease sympathetic vasoconstrictor activity. However, during oral ERT, the decrease in SNA is opposed by sympathetic overactivity related to IGF-I reduction. Because the effects of transdermal ERT are larger than those of oral ERT, the route of administration may be important consideration in optimizing the beneficial effects of ERT on blood pressure and overall cardiovascular health.

estrogen, sympathetic nervous system, blood pressure
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© American Journal of Hypertension, Ltd. 2001
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