AJP - Renal Physiology, Vol 241, Issue 3 224-F230, Copyright © 1981 by American Physiological Society
Prostaglandin-dependent polyuria in hypercalcemia
E. R. Serros and M. A. Kirschenbaum
The present experiments examined the role of prostaglandin biosynthesis in
the increase in urine flow rate seen in rats with hypercalcemia induced by
the administration of 1,25-dihydroxycholecalciferol. In a first group, rats
receiving the vitamin D metabolite developed hypercalcemia, polyuria, and
increased urine prostaglandin E excretion. Indomethacin resulted in a fall
in urine prostaglandin E excretion. A second group was fluid restricted to
ascertain whether increased thirst could be an etiologic mechanism of the
polyuria. This resulted in a trivial fall in urine flow rate despite a fall
in body weight and a rise in both urine and plasma osmolality. In a final
group, prostaglandin inhibition restored the vasopressin sensitivity of the
hypercalcemic kidney. Accordingly, the polyuria seen in hypercalcemic rats
after the administration of 1,25-dihydroxycholecalciferol is associated
with an increase in urine prostaglandin E excretion and can be reversed by
inhibition of prostaglandin synthesis. In addition, this polyuria can occur
independent of the thirst mechanism. Finally, there is evidence that the
vasopressin resistance of the hypercalcemic kidney could be reversed by
prostaglandin inhibition.
