Purpose: To determine the effect of estrogen on endothelium-dependent
relaxation in the cutaneous microcirculation of women. Methods: Three
groups of women participated in the study. Group 1 (n = 20) was premen
opausal and had a mean age of 39 years (range 24-50 years). Group 2 (n
= 9) was postmenopausal and had a mean age of 58 years (range 53-65 y
ears). Group 3 (n = 11) was postmenopausal and taking estrogen replace
ment therapy; the mean age was 53 years (range 43-58 years). Eleven wo
men in group 1 underwent testing twice, once during menstruation (mean
serum estradiol level 73 +/- 30 pg/ml) and once during midcycle (mean
serum estradiol level 268 +/- 193 pg/ml; p = 0.003). Single-point las
er Doppler ultrasound and laser Doppler imaging with a scanner were us
ed to measure vasodilatation in the forearm skin in response to iontop
horesis of 1% acetylcholine (endothelium dependent) and 1% sodium nitr
oprusside (endothelium-independent smooth muscle relaxant). Results: A
ll three groups were matched for body mass index and fasting glucose,
total, high-density Lipoprotein, and low-density lipoprotein cholester
ol and triglyceride levels. All women had normal blood pressure, and n
one smoked. Mean serum estradiol levels were 196 +/- 170 pg/ml (group
1), 35 +/- 12 pg/ml (group 2), and 107 +/- 78 pg/ml (group 3) (p = 0.0
04). Maximum microvascular vasodilatation (percentage increase over ba
seline) in response to acetylcholine was reduced in group 2 (93% +/- 4
3%) compared with group 1 (187% +/- 63%) and group 3 (142% +/- 56%) (p
= 0.001). The response to sodium nitroprusside also was diminished in
group 2 (73% +/- 27%) compared with group 1 (126% +/- 45%) and group
3 (100% +/- 32%) (p = 0.02). Within group 1 the acetylcholine response
was higher during the midcycle phase (186% +/- 31%) compared with the
menstrual phase (147% +/- 57%) (p < 0.05). The sodium nitroprusside r
esponse also was higher during the midcycle phase (144% +/- 31%) compa
red with the menstrual phase (94% +/- 41%) (p < 0.05). Conclusion: The
results indicate that estrogens might enhance endothelium-dependent a
nd endothelium-independent vasodilatation in the microcirculation of w
omen.