17ss oestradiol does not attenuate the response to angiotensin I and II during long term therapy in postmenopausal women

It is thought that oestrogen replacement therapy may reduce the conversion of angiotensin I to angiotensin II in postmenopausal women by inhibiting angiotensin converting enzyme. We sought to determine the effects of 3 months oestrogen replacement therapy (ERT) on the response to angiotensin I and I...

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Veröffentlicht in:Cardiovascular drugs and therapy 2004-01, Vol.18 (1), p.31-36
Hauptverfasser: Jhund, Pardeep S, Dawson, Nuala, Davie, Andrew P, Norrie, John, O'Kane, Kevin P J, McMurray, John J V
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Sprache:eng
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Zusammenfassung:It is thought that oestrogen replacement therapy may reduce the conversion of angiotensin I to angiotensin II in postmenopausal women by inhibiting angiotensin converting enzyme. We sought to determine the effects of 3 months oestrogen replacement therapy (ERT) on the response to angiotensin I and II in postmenopausal women. Eighteen postmenopausal women were randomised to either three months of 2 mg oral oestradiol or placebo in a double blind, placebo controlled, protocol. Change in forearm blood flow (FBF), in response to brachial arterial infusion of increasing concentrations of angiotensin I and angiotensin II was measured, pre-randomisation, after 1 months randomised therapy and after 3 months therapy, using venous occlusion plethysmography. Oestrogen treatment had no effect on baseline FBF. The mean (SD) peak reductions in FBF with 64 pmol/min angiotensin I pre-randomisation, after 1 month and after 3 months treatment with placebo were 62(11), 65(15) and 57(8)%. The corresponding reductions with the peak dose of angiotensin II (16 pmol/min) were 53(8), 48(12) and 47(11)%. In the oestradiol group, the peak responses to angiotensin I were 56(8), 53(11) and 44(29)% pre-randomisation, after 1 months treatment and after 3 months treatment. The corresponding reductions in response to angiotensin II were 37(15), 47(15) and 45(19)%. Oestradiol did not affect the response to either angiotensin I or angiotensin II. This study does not support the idea that ERT might exert a cardioprotective effect through inhibition of the renin-angiotensin system.
ISSN:0920-3206
1573-7241
DOI:10.1023/B:CARD.0000025753.20686.2b