Estrogen Treatment Decreases a-Adrenergic Binding Sites on Rabbit Platelets*
- 1 March 1979
- journal article
- research article
- Published by The Endocrine Society in Endocrinology
- Vol. 104 (3), 722-728
- https://doi.org/10.1210/endo-104-3-722
Abstract
Steroid hormones modulate adrenergic response and receptors in several tissues. Estrogen treatment results in increased uterine a-adrenergic contraction and also increased a-adrenergic receptors, as quantitated by the binding of the radioligand [3H]dihydroergocryptine (DHE). We asked whether the change in a-adrenergic receptors after estrogen treatment was unique to the uterus or was present in platelets, another tissue known to be affected by estrogen. We used DHE in binding studies of rabbit platelet particulates and found that DHE binding was consistent with interactions expected at an a-adrenergic receptor; binding was high affinity (Kd = 2 nM), low capacity (190–360 fmol/mg protein), and competed for stereoselectively by adrenergic agents with a typical α-adrenergic rank order of potency. Therefore, we used DHE to quantitate a-adrenergic receptors on platelets from oophorectomized or estrogen-treated animals. Estrogen administered by a treatment protocol that has previously been described to decrease platelet aggregation in rabbits decreased α-adrenergic binding sites by 40%. The time course of this estrogen-stimulated decrease in a-adrenergic receptors suggested that this effect of estrogen was upon megakaryocytes rather than upon circulating platelets. Furthermore, the decrease in α-adrenergic sites was not attributable to competition for the DHE-binding sites by estrogen or catechol estrogen. The 40% decrease of α-adrenergic binding sites in platelets in estrogentreated rabbits contrasts with a 4-fold increase in myometrial a-adrenergic binding sites in the same animals. The alteration in the number of α-adrenergic binding sites by estrogen in opposite directions in different tissues from the same animal suggests a mechanism by which estrogen may modulate sympathetic response.Keywords
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