To gain further knowledge on the role of ovarian hormones in the regulation of mammary β-adrenergic receptors, virgin animals were killed during the various phases of the estrous cycle as well as after ovariectomy and treatment with sex steroids. β-Adrenergic receptor levels fluctuate in the rat mammary gland during the estrous cycle, with higher receptor numbers during the proestrous and estrous phases of the cycle. Ovariectomy caused an almost 50% loss of β-adrenergic receptor concentration in the mammary gland of virgin rats. Treatment of ovariectomized animals with 17β-estradiol or progesterone alone or in combination for 3 weeks induced a marked increase in β-adrenergic receptor concentration, while administration of the androgen dihydrotestosterone did not modify mammary β-adrenergic binding sites. While levels of β-adrenergic receptors in control lactating animals (10 days of lactation) were elevated, chronic treatment with the dopaminergic-mimetic agent 2α-bromoergocryptine (CB-154; for 7 days) reduced β-adrenergic receptor concentration. Castration of lactating animals decreased β-adrenergic receptor number to approximately 30% of the value in intact controls, while combined withdrawal circulating ovarian hormones and inhibition of plasma PRL levels caused an almost complete inhibition of β-adrenergic receptor concentration. Scatchard analysis of the binding data revealed that the observed alterations in β-adrenergic receptors resulted from changes in the number of β-adrenergic binding sites, with no change in binding affinities. The present findings indicate that the β-adrenergic receptor population of the rat mammary gland is under the control of ovarian hormones and PRL and suggest that circulating or locally released catecholamines could interact with sex steroids and PRL in the regulation of mammary gland growth, differentiation, and activity.
|Number of pages||7|
|Publication status||Published - 1990|
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism