Pathogenesis of hyperprolactinemia in uremic rats.

Experiments have been carried out in order to clarify to what extent the absence of PRL renal catabolism in experimental renal insufficiency is responsible for the high PRL circulating levels. Furthermore, the relative contribution of the glomerular filtration rate and peritubular degradation to PRL renal clearance have been assessed. Circulating PRL basal levels were measured by RIA in sham-operated and intact control rats and in three uremic rat models: urine autoinfusion, bilateral ureteral ligation, and bilateral nephrectomy. Plasma PRL basal levels (nanograms per ml; mean +/- SEM) were increased in sham-operated rats (30.3 +/- 5.1) with respect to control animals (18.5 +/- 2.7; P less than 0.05). Bilaterally nephrectomized animals (66.4 +/- 16.4) and those with bilateral ureteral ligation (69.3 +/- 15.9) developed similar hyperprolactinemia, in contrast to urine-autoinfused rats (20.2 +/- 2.1; P less than 0.005) whose hormone levels were similar to those of control animals. Creatinine levels were markedly elevated and comparable in the three uremic rat groups. The results suggest that: 1) hyperprolactinemia in rats in acute renal insufficiency is due primarily to reduced renal function; 2) PRL renal catabolism in the rat requires a certain rate of glomerular filtration; and 3) PRL peritubular degradation does not seem to be relevant in PRL catabolism by rat kidney.