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Cardiovascular Research 2002 53(3):627-633; doi:10.1016/S0008-6363(01)00498-9
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

Isoproterenol amplifies 17β-estradiol-mediated vasorelaxation: role of endothelium/nitric oxide and cyclic AMP

Hoi Yun Chana, Xiaoqiang Yaoa, Suk Ying Tsanga, Jean-Pierre Bourreaub, Franky Leung Chanc and Yu Huanga,*

aDepartment of Physiology, Chinese University of Hong Kong, Shatin, Hong Kong, China
bDepartment of Physiology, The University of Hong Kong, Hong Kong, China
cDepartment of Anatomy, Chinese University of Hong Kong, Shatin, Hong Kong, China

* Corresponding author. Fax: +852-26-035-022 yu-huang{at}cuhk.edu.hk

Objectives: Estrogen exerts cardiac protection via multiple cellular mechanisms. Estrogen modifies vasodilatation induced by certain relaxants such as β-adrenoceptor agonists. However, little is known whether low concentrations of β-adrenoceptor agonists would reciprocally influence the acute relaxant response to estrogen. The present study was designed to investigate the synergistic interaction between isoproterenol and 17β-estradiol, and the role of endothelium and cyclic AMP-dependent pathway in this interaction. Methods: Changes in vessel tone of the isolated rat mesenteric artery rings were measured using a force–displacement Grass transducer. Results: In 9,11-dideoxy-11{alpha}, 9{alpha}-epoxy-methanoprostaglandin F2{alpha}-preconstricted endothelium-intact rings, 17β-estradiol induced relaxations with pD2 of 5.06±0.06. Pretreatment of endothelium-intact rings with isoproterenol (1–3x10–9 M, 1 h incubation time) significantly enhanced 17β-estradiol-induced relaxation. This effect was inhibited by Rp-cGMPS triethylamine (3x10–6 M), and abolished in the presence of 3x10–5 M NG-nitro-L-arginine methyl ester or in endothelium-denuded rings. The effect of isoproterenol was antagonized by propranolol (3x10–6 M), ICI 118,551 (3x10–6 M), but not by atenolol (10–5 M). Rp-cAMPS triethylamine (3x10–6 M) abolished the effect of isoproterenol. Besides, exposure to 3x10–9 M forskolin for 1 h also potentiated the relaxant response to 17β-estradiol. Conclusion: In endothelium-intact rat mesenteric arteries pretreatment with low concentrations of isoproterenol enhanced the acute relaxant response to 17β-estradiol. This enhancement was dependent on the presence of endothelium and abolished by L-NAME via a β2-adrenoceptor-mediated cyclic AMP-dependent mechanism.

KEYWORDS Adrenergic (ant)agonists; Arteries; Endothelial function; Hormones; Vasoconstriction/dilation


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