ABSTRACT
Estrogen [Estradiol] was administered by intramuscular [i.m] route at 1 mg daily for 5 days into each of a group of rats. In another group of rats, the same dose was administered to each for the same period of time, twenty four hours following the i.m. administration of 5 mg of the cytoplasmic estrogen receptor-blocker [Tamoxifen[. In the first group, serum parathyroid hormone [PTH]level showed statistical significant increase from the control value, whereas total serum calcium concentration revealed statistical significant reduction from the control level. Administration of estrogen following tamoxifen resulted in a decrease in PTH concentration which was statistically insignificant compared to the level obtained when estrogen was administered alone, yet it revealed statistical significant increase compared to the control value. The value for total serum calcium demonstrated statistical significant reduction from the control level and which was not statistically different from the level obtained when estrogen was administered alone. These findings reveal that in the rat, exogenous administration of estrogen stimulates PTH release and lowers total serum calcium. Blocking of the estrogen receptors in parathyroid cells by tamoxifen prior to estrogen administration resulted in an inhibition to the stimulatory effect of estrogen on PTH secretion but which was insignifieant. This might result either from a non-sufficient period of exposure of the estrogen receptors in the parathyroid cells so not allowing complete binding with tamoxifen, or that estrogen acted directly on receptors in parathyroid cells which do not competitively bind tamoxifen. However, the direct stimulatory effect of estrogen in vivo on parathyroid cells awaits further evaluation. However, the hypocalcemia observed in both groups could be possibly mediated through one of two mechanisms: Either estrogen decreases the responsiveness of bone to PTH leading to hypocalcemia, or alternatively estrogen induces a rise in calcitonin level, thus producing hypocalcemia. Hypocalcemia in turn causes a compensatory PTH release. Thus estrogen may consequently serve as an important regulator of PTH and-of calcium homeostasis