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SUMMARYPrevious studies have shown that acute administration of estrogen improves endothelial function in postmenopausal women, but there has been little investigation of the chronic effects of transdermal estrogen replacement therapy. The present study assessed the effect of transdermal estrogen replacement therapy (0.025 mg / day for 4 weeks, the normally applied dosage in Japan) on flow-mediated endothelium-dependent vasodilation of the brachial artery (B-mode ultrasound) and forearm cutaneous blood flow (laser Doppler flowmetry), and plasma hormonal and lipid levels in 12 normolipidemic postmenopausal women. Neither resting vascular diameter, flow-mediated vasodilation, nor time to peak vasodilation, showed significant changes after the estrogen therapy. In contrast, resting forearm cutaneous blood flow decreased significantly after the estrogen therapy. The time to the peak reactive hyperemia in the forearm skin was slightly shortened, and the % change in reactive hyperemia decreased slightly after the therapy. These findings seemed to reflect the inhibition of hot-flush symptoms associated with vasomotor abnormalities in cutaneous tissue. The lack of improvement in flow-mediated vasodilation of the brachial artery despite the inhibitory effect on cutaneous vasomotor abnormalities may be related to the low plasma estradiol concentration obtained with the present transdermal therapy (42.4±15.2 pg / ml), a finding which supports the estrogen threshold hypothesis in hormone replacement therapy. (Jpn Heart J 2001; 42: 307-315) Key words: Estrogen replacement therapy, Endothelial function, Reactive hyperemia, Cutaneous circulation THE risk of cardiovascular disease and metabolic disorders is increased in postmenopausal women. Epidemiological studies have shown that estrogen replacement therapy is associated with a reduction of approximately 50% in the incidence of acute coronary events in postmenopausal women. One of the potential mechanisms may be the lipid-lowering effect of estrogen, although lipid changes alone seem to be insufficient to explain the magnitude of the reported cardioprotective effect. Recent studies [1][2][3][4] have shown that estrogen influences the vascular endothelial expression of nitric oxide synthase, which plays an From