Administration of transdermal estrogen without progestin increases the capacity of plasma and serum to stimulate prostacyclin production in human vascular endothelial cells

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Objective: To determine whether transdermal hormone replacement therapy modifies the ability of plasma or serum to regulate the synthesis of prostacyclin and that of endothelin-1 by cultured human umbilical vein endothelial cells. Design: Prospective, randomized study. Setting: Department of Obstetrics and Gynecology, Helsinki University Central Hospital. Patient(s): Thirteen postmenopausal women with climacteric symptoms. Interventions: Transdermal 17β-E 2 (50 μg/d) continuously combined with norethisterone acetate, (250 μg/d) on days 15–28 of the treatment cycles for 6 months. Main Outcome Measure(s): Levels of prostacyclin’s metabolite 6-keto-prostaglandin F 1α and of endothelin-1 released by cultured human umbilical vein endothelial cells. Result(s): Plasma and serum during the E 2-only phase of hormone replacement therapy enhanced prostacyclin production by 20% ± 8% (mean ± SEM) and 23% ± 11%, respectively. Plasma or serum taken during the E 2 + norethisterone acetate phase failed to affect prostacyclin production. Hormone replacement therapy induced no change in the capacity of plasma or serum to release endothelin-1. Conclusion(s): Transdermal hormone replacement therapy during the E 2-only phase increased the capacity of plasma and serum to enhance production of vasoprotective prostacyclin in human vascular endothelial cells, without affecting production of endothelin-1. Addition of norethisterone acetate prevented this stimulation.