title: Administration of transdermal estrogen without progestin increases the capacity of plasma and serum to stimulate prostacyclin production in human vascular endothelial cells.
abstract: 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.
  
  
  METHODS
  Prospective, randomized study.
  
  
  METHODS
  Department of Obstetrics and Gynecology, Helsinki University Central Hospital.
  
  
  METHODS
  Thirteen postmenopausal women with climacteric symptoms.
  
  
  METHODS
  Transdermal 17beta-E2 (50 microg/d) continuously combined with norethisterone acetate, (250 microg/d) on days 15-28 of the treatment cycles for 6 months.
  
  
  METHODS
  Levels of prostacyclin's metabolite 6-keto-prostaglandin F1alpha and of endothelin-1 released by cultured human umbilical vein endothelial cells.
  
  
  RESULTS
  Plasma and serum during the E2-only phase of hormone replacement therapy enhanced prostacyclin production by 20% +/- 8% (mean +/- SEM) and 23% +/- 11%, respectively. Plasma or serum taken during the E2 + 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.
  
  
  CONCLUSIONS
  Transdermal hormone replacement therapy during the E2-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.
authors.affiliation: Department of Obstetrics and Gynecology, Helsinki University Central Hospital, Finland. tomi_mikkola@hotmail.com
authors.forename: T
authors.initials: T
authors.lastname: Mikkola
authors.forename: L
authors.initials: L
authors.lastname: Viinikka
authors.forename: O
authors.initials: O
authors.lastname: Ylikorkala
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism; D000279:Administration, Cutaneous; D001769:Blood; D002478:Cells, Cultured; D019332:Endothelin-1 / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism*; D011464:Epoprostenol / Q000096:biosynthesis*; D004958:Estradiol / Q000008:administration & dosage* / Q000097:blood; D015914:Estrogen Replacement Therapy; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D006801:Humans; D009640:Norethindrone / Q000008:administration & dosage / Q000031:analogs & derivatives; D000077563:Norethindrone Acetate; D017698:Postmenopause; D011372:Progestins / Q000008:administration & dosage*; D011446:Prospective Studies; D014471:Umbilical Veins
chemical_list: D019332:Endothelin-1; D011372:Progestins; D004958:Estradiol; D015121:6-Ketoprostaglandin F1 alpha; D005640:Follicle Stimulating Hormone; D000077563:Norethindrone Acetate; D011464:Epoprostenol; D009640:Norethindrone