title: Arterial reactivity is enhanced in genetic males taking high dose estrogens.
abstract: OBJECTIVE
  We sought to assess whether high dose estrogen treatment is associated with enhanced arterial reactivity in genetic males.
  
  
  BACKGROUND
  Although estrogens have been shown to enhance arterial reactivity in women, and are thereby thought to confer cardiovascular benefit, the vascular effects of long-term estrogen therapy in genetic males is unknown.
  
  
  METHODS
  We studied the arterial physiology of 30 genetic males--15 male to female transsexuals receiving long-term high dose estrogen therapy and 15 healthy male control subjects matched for age, smoking history and vessel size. Using external vascular ultrasound, brachial artery diameter was measured at rest, after flow increase (causing endothelium-dependent dilation [EDD]) and after nitroglycerin (GTN), an endothelium-independent dilator. Blood pressure, cholesterol and testosterone levels were also measured in each subject.
  
  
  RESULTS
  Total testosterone and free testosterone index levels were lower in the transsexuals compared with the control subjects (p < 0.001). In contrast, EDD was significantly higher in the transsexuals than in the control males (mean [+/-SD] 7.1 +/- 3.1% vs. 3.2 +/- 2.8%, p = 0.001), as was the GTN response (21.2 +/- 6.7% vs. 14.6 +/- 3.3%, p = 0.002). Total and high density lipoprotein cholesterol, blood pressure levels and baseline vessel size were similar in the two groups. On multivariate analysis, enhanced EDD was associated independently with estrogen therapy (p = 0.02) and with low total cholesterol (p = 0.04). An enhanced GTN response was also significantly associated with estrogen therapy (p = 0.03).
  
  
  CONCLUSIONS
  Long-term treatment with high dose estrogens is associated with enhanced arterial reactivity in genetic males, which may be due to the effects of estrogen excess or androgen deprivation, or both.
authors.affiliation: Department of Cardiology, Royal Prince Alfred Hospital, Sydney, Australia.
authors.forename: J A
authors.initials: JA
authors.lastname: McCrohon
authors.forename: W A
authors.initials: WA
authors.lastname: Walters
authors.forename: J T
authors.initials: JT
authors.lastname: Robinson
authors.forename: R J
authors.initials: RJ
authors.lastname: McCredie
authors.forename: L
authors.initials: L
authors.lastname: Turner
authors.forename: M R
authors.initials: MR
authors.lastname: Adams
authors.forename: D J
authors.initials: DJ
authors.lastname: Handelsman
authors.forename: D S
authors.initials: DS
authors.lastname: Celermajer
mesh_terms: D000328:Adult; D001808:Blood Vessels / Q000187:drug effects* / Q000502:physiology; D001916:Brachial Artery / Q000187:drug effects; D003430:Cross-Sectional Studies; D004730:Endothelium, Vascular / Q000187:drug effects*; D045166:Estradiol Congeners / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D012039:Regional Blood Flow; D014189:Transsexualism; D014664:Vasodilation / Q000187:drug effects
chemical_list: D045166:Estradiol Congeners