Parathyroid hormone secretion: Effect of estradiol and progesterone

Abstract

Previous studies have shown that estrogen therapy in postmenopausal women results in an increase in serum immunoreactive parathyroid hormone (iPTH) levels. It has been assumed that this effect of estrogen on PTH secretion is indirect, being mediated via mild hypocalcemia resulting from an inhibition of bone resorption. We evaluated the direct effect of 17 β-estradiol (E 2) and of progesterone (Prog) on secretion of PTH from bovine parathyroid tissue in vitro. Both E 2 and Prog caused a significant stimulation of PTH secretion within one hour, which was progressive for the three-hour observation period. The responses were dose-related from 10 −7 to 5 × 10 −10 mol/L. There was no PTH response to 10 −7 mol/L α-E 2, 3-methoxy estriol, estrone, testosterone, or 20-α-hydroxy progesterone, indicating specificity of the responses to E 2 and Prog. There was a minimal PTH secretory response to 10 −8 mol/L cortisol and 10 −6 mol/L estrone. The E 2 receptor antagonist tamoxifen did not inhibit the E 2 effect on PTH secretion. This observation plus the rapid PTH response suggests that this hormonal effect may not be via the conventional intracellular E 2 receptor. Therefore, E 2 and Prog can stimulate PTH secretion by rapid, direct, and specific effects on parathyroid cells. These gonadal hormones may, therefore, be important in calcium homeostasis via their direct stimulatory effect on PTH secretion.