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Estrogens directly down-regulate receptors for angiotensin II in anterior pituitary cell culture without decreasing target cell responsiveness.

Chronic estradiol treatment in vivo has been shown to reduce the density of receptors for angiotensin II (ANG II) in the anterior pituitary lobe (AP). We studied whether estradiol is directly involved in the down-regulation of ANG II receptors, using AP cells in culture. Binding affinity and density of ANG II receptors were measured in disrupted AP cells with the radiolabeled antagonist [125I]Sar1, Ile8-ANG II ([125I]SARILE). Estradiol treatment (10 nM) for either 48 or 96 h caused a marked reduction (approximately 70%) in the density of receptors for ANG II in cultured AP cells, with no change in the dissociation constant of [125I]SARILE (Kd, 0.5 +/- (SE) 0.1 nM). In the AP, specific binding sites for ANG II are present in lactotrophs and ANG II has been shown to release prolactin (PRL). In AP cells treated with estradiol for 48 h, dose-response curves revealed that ANG II still increased PRL release (P less than 0.01). The average net PRL release (ANG II-stimulated minus basal) was greater in estradiol-treated cells than in controls, whereas the half-maximal stimulation dose (ED50) of ANG II was the same (0.07 +/- 0.04 nM). These results suggest that estrogens are directly involved in the modulation of ANG II receptors in the AP, causing marked receptor down-regulation without decreasing target cell responsiveness.