Open AccessEstrogen affects vascular tone differently according to vasoactive substances in ovariectomized Sprague-Dawley rat
Author(s) -
Bonggwan Seo,
Koji Ikeda,
Noriaki Emoto,
Dong Ju Choi,
Jin Yong Hwang,
Masafumi Matsuo,
Young Ho Kim,
Il Seok Cheon
Publication year - 2000
Publication title -
yonsei medical journal/yonsei medical journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.702
H-Index - 63
eISSN - 1976-2437
pISSN - 0513-5796
DOI - 10.3349/ymj.2000.41.1.49
Subject(s) - endocrinology , medicine , ovariectomized rat , angiotensin ii , estrogen , endothelin receptor , contraction (grammar) , vascular smooth muscle , vasodilation , estrogen receptor , angiotensin ii receptor type 1 , chemistry , receptor , cancer , smooth muscle , breast cancer
The favorable effects of estrogen on cardiovascular diseases can be explained by several mechanisms such as changes in serum lipid profiles and thrombogenecity. Estrogen also affects the vascular tone, but there has been no report in which the effect of estrogen was tested comprehensively for several vasoactive substances, especially after long-term administration. Two weeks after bilateral ovariectomy in 8-week old female Sprague-Dawley rats, placebo or 17 beta-estradiol (E2) pellets (0.5 mg; released over 3 weeks) were implanted subcutaneously. Two weeks after pellet implantation, organ chamber experiments were performed using aortae. Compared with control, E2-treated vessels showed impaired endothelium-dependent relaxation to acetylcholine. E2 enhanced the contraction to norepinephrine and U46619 and had no effect on endothelin-1-induced contraction. In contrast, the contraction to angiotensin (AT)-II was inhibited by E2. Northern blot analysis for AT1 receptor expression using cultured aortic smooth muscle cells showed no difference between control and E2-treated cells, suggesting that AT1 receptor downregulation is not the likely mechanism. These results suggest that E2 affects the vascular tone variably according to vasoactive substances.