Increased water excretion in hyperprolactinemic rats.
The role of PRL in mammalian salt and water balance remains controversial. To avoid the methodological problems of exogenous PRL administration, endogenous hyperprolactinemia was established in normal rats by implantation of extra anterior pituitary glands under the kidney capsule. To eliminate excess glucocorticoid secretion in these rats, they were adrenalectomized, implanted with corticosterone replacement pellets, and given 0.9% saline drinking fluid. A highly significant increase in urine flow was found in pituitary-grafted male Fischer rats compared to control rats (38.9 +/- 3.8 vs. 20.7 +/- 1.6 ml/24 h X 100 g BW; P less than 0.0005). Urine osmolality was lower in pituitary-grafted rats, but sodium and potassium excretion were not abnormal. Although fluid intake was also greater in hyperprolactinemic rats, the urine flow remained elevated when adjusted for fluid intake. Renal binding sites for radioactive PRL were not decreased in pituitary-grafted rats. Thus, the hyperprolactinemic rat has increased water excretion that may be attributed to a direct renal effect rather than to glucocorticoid excess or a primary change in thirst. Since it is possible that water absorption in the gut is also increased by PRL, multiple effects of PRL may be responsible for the diuresis observed in hyperprolactinemic rats.
D000818:Animals; D001971:Bromocriptine / Q000494:pharmacology; D003345:Corticosterone / Q000652:urine; D004231:Diuresis; D005260:Female; D006966:Hyperprolactinemia / Q000378:metabolism*; D008297:Male; D009132:Muscles / Q000637:transplantation; D010903:Pituitary Gland, Anterior / Q000637:transplantation; D011388:Prolactin / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D011956:Receptors, Cell Surface / Q000378:metabolism; D011981:Receptors, Prolactin
D011956:Receptors, Cell Surface; D011981:Receptors, Prolactin; D001971:Bromocriptine; D011388:Prolactin; D003345:Corticosterone