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Endothelin levels decrease after oral and nonoral estrogen in postmenopausal women with increased cardiovascular risk
J G Wilcox1, I E Hatch, E Gentzschein
1Department of Obstetrics and Gynecology, University of Southern California School of Medicine, Los Angeles, USA.
Objective:
To establish levels of plasma endothelin-1 in postmenopausal women with increased CV risk as compared with healthy premenopausal women and to measure the effects of different forms of estrogen replacement on plasma endothelin-1.
Design:
Prospective randomized study.
Setting:
University of Southern California Medical Center.
Patient(S):
We studied 18 postmenopausal women (mean age 53.4 +/- 4.9 years) with total cholesterol levels > 240 mg/dL divided into those with and without hypertension as well as in 10 healthy premenopausal women.
Intervention(S):
The postmenopausal women were randomized to receive oral estrone sulfate, transdermal E2, or placebo for 30 days.
Main Outcome Measure(S):
We measured the endothelin-1 levels and total cholesterol at baseline and after 30 days of estrogen treatment.
Result(S):
In the postmenopausal women, endothelin-1 was higher (4.58 +/- 0.46 pg/mL) compared with premenopausal levels (2.80 +/- 0.46 pg/mL). In hypertensive postmenopausal women, endothelin-1 was 5.56 +/- 0.44 pg/mL. After estrogen, plasma endothelin-1 values decreased from 5.38 +/- 0.66 to 4.82 +/- 0.9 pg/mL with oral estrone sulfate, 4.84 +/- 0.25 to 4.54 +/- 0.49 pg/mL with transdermal E2, and did not change after placebo 4.76 +/- 0.71 to 4.81 +/- 0.46 pg/mL. In evaluating hypertensive women alone with estrogen therapy, plasma endothelin-1 showed the greatest decrement from 5.39 +/- 0.49 to 4.4 +/- 0.59 pg/mL (18.4%). The decrease in endothelin-1 with estrogen, which was statistically significant for the entire group, did appear to be influenced by the route of administration. Baseline plasma endothelin-1 levels were correlated positively to plasma cholesterol levels with a correlation coefficient of 0.632.
Conclusion(S):
These data provide another potential mechanism explaining the cardioprotective effects of hormone replacement therapy.