Hot flashes are among the most common complaints of perimenopausal women. D
espite the high prevalence of the phenomenon, the background to the develop
ment of hot flashes is still not completely understood, through a hypothesi
zed central mechanism, involving norepinephrine and luteinizing hormone-rel
easing hormone (LH-RH) secretion is widely accepted. We studied the influen
ce of sex steroid deficiency and hormone replacement therapy on the biomech
anical properties of musculocutaneous arterioles, to see whether a peripher
al mechanism also exists in the development of hot flashes.
Fifty adult, nulliparous, non-pregnant female Sprague-Dawley rats received
pharmacological ovariectomy, and estradiol, medroxyprogesterone, or both ho
rmones. After 12 weeks the saphenous artery was isolated by microdissection
. Norepinephrine-induced tone (active tangential strain) was measured as a
function of intraluminal pressure in an organ bath.
The norepinephrine-induced arterial tone was significantly different betwee
n the control group and the ovariectomized animals in the range of 80-150 m
mHg intraluminal pressure (p < 0.05). Also, significant differences were fo
und between the ovariectomized group and the animals receiving estradiol mo
notherapy (p < 0.01 between 80 and 170 mmHg, and p < 0.05 between 180 and 2
00 mmHg intraluminal pressure). Neither medroxyprogesterone combined hormon
e replacement therapy induced significant changes in the norepinephrine-ind
uced vascular tone.
The absence of sex steroids leads to decreased reactivity to norepinephrine
in small musculocutaneous arteries, while chronic estradiol replacement th
erapy restores the impaired responsiveness of the vessels. Our data raise t
he possibility that in addition to tie central mechanism, a previously unkn
own peripheral background mechanism for perimenopausal hot flashes ray exis
t.