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Cardiovascular Research 1999 42(1):224-231; doi:10.1016/S0008-6363(98)00265-X
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Short-term exposure to physiological levels of 17β-estradiol enhances endothelium-independent relaxation in porcine coronary artery1

Hwee Teoh*, Susan W.S. Leung and Ricky Y.K. Man

Department of Pharmacology, Faculty of Medicine, The University of Hong Kong, 1/F Li Shu Fan Building, 5 Sassoon Road, Hong Kong, PR China

* Corresponding author. Tel.: +852-2819-9103; fax: +852-2817-0859. E-mail address: hteoh@hkusua.hku.hk (H. Teoh)

Objectives: While alterations in cholesterol and lipoprotein profiles partly account for menopause being a risk factor for coronary heart disease, recent studies have suggested that 17β-estradiol may have vascular effects. Our aims were to study the short-term effects of 17β-estradiol on vascular function in isolated porcine coronary artery rings. Concomitantly, we sought to determine if physiological concentrations of 17β-estradiol could acutely potentiate relaxation. Results: 17{alpha}- and 17β-estradiol at pharmacological (>1 µM) concentrations produced relaxation in U46619 [GenBank] -pre-contracted porcine coronary artery rings. Relaxation evoked by 17β-estradiol was not reversed by the estrogen receptor antagonists tamoxifen and ICI 182780. Following 20 min exposure to a physiological concentration of 17β-estradiol (1 nM), which on its own had no effect, relaxation elicited by cromakalim, levcromakalim and sodium nitroprusside, but not bradykinin or calcium ionophore A23187 [GenBank] , were significantly enhanced. This potentiating action was also insensitive to tamoxifen and ICI 182780. Our data provide evidence for an acute indirect relaxant action of 17β-estradiol and suggest that it may be via a tamoxifen- and ICI 182780-insensitive estrogen receptor. While this response was only observed at pharmacological concentrations, the potentiation of cromakalim, levcromakalim and sodium nitroprusside relaxation was evident in the presence of a physiological concentration (1 nM) of 17β-estradiol. Conclusions: These results demonstrate that short-term exposure to 17β-estradiol, at concentrations that have no effect on their own, can enhance vasorelaxation. These vascular effects may partly account for some of the acute effects of 17β-estradiol on blood flow.

KEYWORDS Estradiol; Vessel; Coronary; Vasodilation; Swine

1 See pages 9–11.


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