Estrogen improves impaired musculocutaneous vascular adrenergic reactivityin pharmacologically ovariectomized rats: a potential peripheral mechanismfor hot flashes?

Citation
N. Acs et al., Estrogen improves impaired musculocutaneous vascular adrenergic reactivityin pharmacologically ovariectomized rats: a potential peripheral mechanismfor hot flashes?, GYNECOL END, 15(1), 2001, pp. 68-73
Citations number
17
Categorie Soggetti
Reproductive Medicine
Journal title
GYNECOLOGICAL ENDOCRINOLOGY
ISSN journal
09513590 → ACNP
Volume
15
Issue
1
Year of publication
2001
Pages
68 - 73
Database
ISI
SICI code
0951-3590(200102)15:1<68:EIIMVA>2.0.ZU;2-3
Abstract
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.