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Preserved Forearm Endothelial Responses with Acute Exposure to Progesterone: A Randomized Cross-Over Trial of 17-ß Estradiol, Progesterone, and 17-ß Estradiol with Progesterone in Healthy Menopausal Women¹

Division of Endocrinology (K.J.M.), Indiana University School of Medicine, Indianapolis, Indiana; and University of British Columbia and Vancouver Hospital and Health Sciences Centre (E.G.N., J.C.P., T.G.E.), Department of Medicine, Division of Endocrinology and Metabolism, Vancouver, British Columbia, Canada V5Z 1C6

Address all correspondence and requests for reprints to: T. G. Elliott, M.B.B.S., FRCPC, Suite 380, 575 West 8th Avenue, Vancouver, British Columbia, Canada V5Z 1C6.

Regularly menstruating women are relatively protected from cardiovascular disease. Epidemiological and endothelial function studies attribute this protection to estradiol (E₂), but both progesterone (P) and E₂ are normally present. A range of vascular effects of added progestins have been described, from neutral to detrimental, but the effects of P per se on endothelial function in humans have not been reported. We therefore investigated the acute effects of E₂, P, and E₂ combined with P, on endothelium-dependent and -independent forearm blood flow responses.

Using venous occlusion plethysmography, forearm blood flow (FBF) was measured during acute brachial artery infusions, achieving physiologic levels of 17-ß-E₂, P, and 17-ß-E₂ with P in healthy menopausal women with no cardiovascular disease risk factors. Vehicle or hormones were infused, in random order, on 4 days, 1 week apart. Flow responses were measured during coinfusions of hormone with the endothelium-dependent vasodilator acetylcholine and the endothelium-independent vasodilator sodium nitroprusside.

Twenty-seven healthy menopausal women were studied, and all had normal baseline endothelial responses. Small (15%), statistically nonsignificant increases in endothelium-dependent flow responses were seen after all acute hormone treatments. No impairment in response was seen with P alone or in combination with 17-ß-E₂.

In healthy menopausal women without cardiovascular disease risk factors and without baseline defects in endothelial function, acute exposure to physiologic levels of 17-ß-E₂, P, and 17-ß-E₂ with P produced equivalent endothelium-dependent responses. These data suggest that P does not have detrimental vascular effects in humans.

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