Affiliation:
1. Hypertension Unit, Department of Clinical Pharmacology, Royal North Shore Hospital, St Leonards, New South Wales, Australia
2. Department of Statistics, Royal North Shore Hospital, St Leonards, New South Wales, Australia
3. Department of Obstetrics and Gynaecology, Royal North Shore Hospital, St Leonards, New South Wales, Australia
Abstract
1. Studies were undertaken in pre-menopausal women to examine the effects of treatment with standard oestrogen-progestogen and progestogen-only oral contraceptives on erythrocyte Na+,K+ co-transport and Na+−Na+ countertransport over 3- and 6-month periods. Concurrent observations were made on other erythrocyte cation transport components, plasma lipid concentrations, plasma renin activity, plasma aldosterone concentration and blood pressure.
2. Na+,K+ co-transport, measured as the ouabain-resistant, frusemide-sensitive component of 86Rb+ influx, and Na+−Na+ countertransport, measured as the ouabain-resistant, phloretin-sensitive component of 22Na+ influx, were both increased in women taking, on days 1–21 of their cycle, ethinyloestradiol (30–50 μg) combined with norethisterone (1000 μg or 500–1000 μg) for 3 or 6 months. Neither of these fluxes was increased in a control group of women, or in women treated for the same time periods with ethinyloestradiol combined with levonorgestrel.
3. In a separate study of erythrocyte cation transport (excluding Na+−Na+ countertransport), in which women undertook treatment with norethisterone only (350 μg/ day) for 6 months starting 6 weeks post partum, no changes in Na+,K+ co-transport were observed at 3 or 6 months; there were no changes in cation transport in a corresponding control group.
4. The results of these studies confirm that certain oral contraceptive compounds can alter erythrocyte cation transport, and indicate that norethisterone in higher dose preparations is the component predominantly responsible. The alterations observed could not be explained by a direct link with concurrent changes in plasma triacylglycerol concentrations or in the renin-aldosterone axis and were not closely associated with elevation of blood pressure.
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