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Effects of exogenous female sex‐steroid hormones on lymphocyte β 2 ‐adrenoceptors in normal females
Author(s) -
TAN K. S.,
McFARLANE L. C.,
COUTIE W. J.,
LIPWORTH B. J.
Publication year - 1996
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1046/j.1365-2125.1996.3311.x
Subject(s) - endocrinology , medicine , luteal phase , follicular phase , menstrual cycle , hormone , medroxyprogesterone , estrogen , medroxyprogesterone acetate , receptor , biology
We have previously shown that lymphocyte β 2 ‐adrenoceptors (AR) are under cyclical control of sex‐steroid hormones with greater receptor density during the luteal phase of the menstrual cycle. It has also been postulated that abnormal cyclical regulation of β 2 ‐AR might be a possible mechanism for premenstrual asthma. The effects of exogenous female sex‐steroid hormones on lymphocyte β 2 ‐AR function were studied in eight normal healthy females. They were evaluated at two successive menstrual cycles, during the follicular phase (day 1–6). They were randomized to receive single oral doses of either ethinyloestradiol 50 μg or medroxyprogesterone 10 mg in a cross‐over study. Lymphocyte β 2 ‐AR parameters were evaluated at baseline ( t 0 ), 24 h ( t 24 ) and 72 h ( t 72 ) after ingestion. Baseline levels of progesterone and oestradiol were comparable on both cycles. Receptor density (B max ) increased significantly ( P <0.01) from t 0 after progesterone but not oestradiol at t 24 : a 1.39‐fold geometric mean difference (95% CI 0.96–2.00) between t 24 vs t 0 . Receptor affinity ( K d ) and maximal cAMP response to isoprenaline (E max ) were not altered by either treatment. These results show that exogenous progesterone but not oestradiol, given during the follicular phase, significantly increased β 2 ‐AR. This, therefore, suggests that endogenous progesterone is probably responsible for previously observed increase in B max during the luteal phase of the female menstrual cycle. These findings may suggest possible therapeutic strategies for modulation of β 2 ‐AR in premenstrual asthma.