There is evidence that
prolactin (PRL) excess plays a role in the etiology of
osteoporosis associated with human
prolactinoma.
Calcium balance in human
hyperprolactinemia has not been thoroughly investigated. In the present study, rats with excess circulating PRL levels (male anterior pituitary-grafted Fischer 344 rats) had urinary
calcium excretion twice that of control rats (4.16 +/- 0.43 v 2.25 +/- 0.30 mg/24h X 100 g BW).
Calcium excretion expressed per mg of
calcium intake was also high in pituitary-grafted rats. The excess
calcium excretion in hyperprolactinemic rats was not accompanied by a concomitant rise in
sodium excretion. This dissociation suggests that PRL has an effect on the renal handling of
calcium. Since
thiazide diuretics have a well-described hypocalciuric action, their effect was tested in these rats. In normal rats,
benzthiazide, a long-acting agent, significantly reduced urinary
calcium excretion in a dose-dependent fashion. Hyperprolactinemic rats responded to
benzthiazide in a manner similar to control rats. In pituitary-grafted rats,
benzthiazide also decreased the
calcium excretion to intake ratio and normalized the
calcium to
sodium excretion ratio. Since the
hypercalciuria of experimental
hyperprolactinemia can be corrected by
thiazide diuretics, these agents may have therapeutic potential in human PRL excess.