Mineralocorticoid modulation of prolactin effect on renal solute excretion in the rat.

Abstract

The effects of ovine PRL (oPRL) on renal solute and water handling were examined in 1) intact, 2) salt-loaded (6 meq NaCl ip X 8 days), 3) adrenalectomized (adx), 4) adx plus corticosterone-treated (133 micrograms/100 g BW im), and 5) adx plus dexamethasone-treated (10 micrograms/100 g BW im) male rats. After 7 days treatment rats received a water load (3% BW ip) before a 4-h urine collection. Rats also received 0.9% NaCl im (controls) or 1.0 mg oPRL on days 4-7. Treatments were continued to day 8 for inulin clearance determination. The effects of arginine vasopressin (AVP) (173 microU im, days 4-7) on renal solute and water excretion were also examined in salt-loaded rats to see if renal effects of oPRL treatment were due to AVP contamination of the oPRL preparation. In intact rats drinking tap water, oPRL decreased sodium clearance (CNa) and potassium clearance (CK) (P less than 0.05) vs. controls, with no change in free water clearance (CH2O). In intact rats receiving 1.0% NaCl and 1.0% glucose as a replacement for drinking water, oPRL decreased CNa (P less than 0.05) and increased CK (P less than 0.05) vs. controls, with no change in osmolar clearance or CH2O. In salt-loaded rats oPRL increased CNa and CK (P less than 0.05) vs. controls, with no change in CH2O. AVP administration to salt-loaded rats, however, had no effect on CNa and decreased CK vs. controls. oPRL increased CK (P less than 0.05) in adx rats, with no effect on CNa. In adx plus corticosterone-treated rats oPRL decreased CNa and CK (P less than 0.005), similar to its effect in intact animals. oPRL had no effect on renal solute or water excretion as compared to control animals in dexamethasone-treated adx rats. oPRL did not alter glomerular filtration rate at any time. These data suggest that 1) oPRL requires the presence of mineralocorticoids for an effect on sodium, but not potassium, excretion, 2) elevated sodium intake reverses the effect of oPRL on potassium excretion, 3) oPRL potentiates the effects of corticosterone on sodium reabsorption, and 4) glucocorticoids may block the effects of oPRL on the kidney.