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Human Reproduction, Vol. 17, No. 7, 1918-1924, July 2002
© 2002 European Society of Human Reproduction and Embryology

Is estradiol cardioprotection a nitric oxide-mediated effect?

A.C. Duncan1, J.R. Petrie2, M.J. Brosnan2, A.M. Devlin2, R.A. Bass3, D.S. Charnock-Jones3, J.M.C. Connell2, A.F. Dominiczak2 and M.A. Lumsden1,4

1 University Departments of Obstetrics and Gynaecology, Queen Mother's Hospital, Yorkhill, Glasgow G3 8SJ, 2 Medicine and Therapeutics, Western Infirmary, Glasgow and 3 Obstetrics and Gynaecology, The Rosie Hospital, Cambridge, UK

BACKGROUND: Estradiol exerts a number of biological effects that support extensive observational data suggesting a protective role for estrogen in cardiovascular disease prevention. These include effects on lipid and carbohydrate metabolism, coagulation/fibrinolysis as well as a possible effect on vascular reactivity. It has been proposed that this might be mediated by vascular endothelial nitric oxide (NO) production. Accordingly, we designed complementary in-vivo and in-vitro studies to investigate this hypothesis further. METHODS: Firstly, in a group of 10 healthy post-menopausal women, bilateral venous occlusion plethysmography was used to examine forearm vasoconstrictor responses to intrabrachial NG-monomethyl-l-arginine (l-NMMA; a substrate inhibitor of nitric oxide synthase) both before and after 4 weeks of treatment with transdermal 17ß-estradiol (E2) (80 µg/day). Secondly, we examined the direct effects of acute (24 h) and chronic (7 days) treatment with E2 (10 pmol/l and 10 nmol/l) on endothelial nitric oxide synthase (eNOS) gene expression in cultured human aortic endothelial cells. RESULTS: No significant differences were observed between the vasoconstrictor responses to l-NMMA (2, 4, 8 µmol/min) before and after E2 treatment. Comparison of E2-treated endothelial cells with control cells showed no significant increase in eNOS mRNA expression following either acute or chronic estradiol treatment. CONLUSIONS: The present studies do not provide evidence for an eNOS-mediated cardioprotective response to estrogen and therefore suggest that additional mechanisms other than the endothelial NO system may have an important role in the cardiovascular effects of estrogen.

Key words: cardiovascular disease/hormone replacement therapy/menopause/nitric oxide/oestrogen

4 To whom correspondence should be addressed. E-mail: M.A.Lumsden{at}clinmed.gla.ac.uk


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