G. New et al., Acute administration of 17 beta-oestradiol does not improve endothelium-dependent vasodilatation in young men, CLIN SCI, 97(2), 1999, pp. 225-232
Studies have recently demonstrated that long-term oestrogen therapy improve
s endothelium-dependent and endothelium-independent vasodilatation in the c
onductance vessels of biological males. We sought to determine if an acute
single dose of oestrogen might similarly improve vasodilator function in yo
ung males. in a randomized, double-blind, placebo-controlled, crossover stu
dy, we compared the effects of 1 mg of sublingual 17 beta-oestradiol (E-2)
and placebo on endothelium-dependent and endothelium-independent vasodilata
tion in the brachial artery using a non-invasive ultrasound technique. We r
ecruited 30 young males based on a power calculation. Neither acute subling
ual oestrogen nor placebo affected flow-mediated vasodilatation [5.32 +/- 0
.78% and 5.28 +/- 0.60% respectively (mean +/- S.E.M.), P = 0.94]. Response
s to nitroglycerine were similar after oestrogen or placebo (16.01 +/- 0.86
% and 15.29 +/- 1.19%, P = 0.47). Basal blood flow and flow during reactive
hyperaemia did not differ after oestrogen or placebo. Heart rate and blood
pressure were similar during both treatment phases of the study. The absol
ute change in serum oestradiol levels was greater after the oestrogen treat
ment phase than after placebo (1509 +/- 87 versus -13 +/- 4 pmol/l, P < 0.0
001). Despite achieving supraphysiological oestradiol levels, the acute adm
inistration of sublingual E-2 does not appear to improve endothelium-depend
ent or endothelium-independent vasodilatation, at least acutely, in the bra
chial artery of young males. In keeping with our previous study, these data
suggest that a period of oestrogen 'priming' (possibly to induce receptor-
mediated nitric oxide synthesis) may be required to yield an improvement in
vascular function in males.