PROGESTIN ENHANCES VASOCONSTRICTOR RESPONSES IN POSTMENOPAUSAL WOMEN RECEIVING ESTROGEN REPLACEMENT THERAPY

Citation
Jm. Sullivan et al., PROGESTIN ENHANCES VASOCONSTRICTOR RESPONSES IN POSTMENOPAUSAL WOMEN RECEIVING ESTROGEN REPLACEMENT THERAPY, Menopause, 2(4), 1995, pp. 193-199
Citations number
29
Categorie Soggetti
Obsetric & Gynecology","Reproductive Biology
Journal title
ISSN journal
10723714
Volume
2
Issue
4
Year of publication
1995
Pages
193 - 199
Database
ISI
SICI code
1072-3714(1995)2:4<193:PEVRIP>2.0.ZU;2-L
Abstract
Clinical and experimental evidence suggests that the cardioprotective effect of estrogen replacement is due to effects both on serum lipids and on blood vessels. Current practice includes the use of a progestin in combination with estrogen if the patient still has her uterus; how ever, little is known about the effects of combination therapy on vasc ular reactivity. We therefore studied the effects of estrogen alone an d with added progestin on forearm vascular resistance at rest, during reactive hyperemia, and after cold presser stimulation using plethysmo graphy in six healthy, postmenopausal women. Measurements were made be fore therapy; after giving conjugated estrogen i.v.; followed by a dai ly oral dose of 0.625 mg for 21 days; and sequentially after the addit ion of 10 mg of medroxyprogesterone acetate (MPA) for 10 days. Mean bl ood pressure did not change significantly. After 21 days of estrogen t herapy, forearm blood flow, resting vascular resistance, and resistanc e after cold presser stimulation did not change significantly. However , after addition of MPA, resting forearm vascular resistance rose sign ificantly from baseline: 25.7 +/- 2.7 U (SE) versus 38.3 +/- 2.5 (p = 0.004). In addition, forearm vascular resistance rose to a higher leve l after cold presser stimulus during combination therapy (32.3 +/- 5.9 vs. 58.4 +/- 5.7; p = 0.0057) than after estrogen replacement alone ( 32.3 +/- 5.9 vs. 37.7 +/- 5.3; p = NS). We conclude that combination h ormone replacement therapy results in higher resting vascular resistan ce and increased presser responsiveness than does estrogen replacement therapy alone.