The principal physiological effect of the anterior pituitary hormone prolactin is to stimulate milk production during lactation. However, recombinant mouse prolactin (PRL) has recently been shown to have an antidiuretic effect when the normal antidiuretic hormone, vasopressin, is either absent from the circulation or its secretion inhibited(1). The present study was designed to investigate whether this antidiuretic effect of prolactin was mediated by changes in the glomerular filtration rate (GFR). Anaesthetized adult male Sprague Dawley rats were surgically prepared for urine collection and cardiovascular monitoring, and fluid-loaded by infusing hypotonic saline (75 millimoles per litre NaCl) intravenously at a rate of 15 millilitres per hour. The GFR was determined using 3H-inulin clearance before, during and after the iv. sequential infusion of two doses of PRL (20, 40 micrograms per millilitre in 150 millimolar NaCl at 0.5 millilitres per hour per 100g, each for 90 min, n=8) or vehicle alone (controls, n=7). Significant (P<0.05) decreases in urine flow and sodium excretion were observed in the treated animals with the higher dose of PRL compared with the controls. However, there was no significant alteration in GFR throughout the study period in either the PRL-treated rats (3.1 plus/minus 0.2, 2.9 plus/minus 0.2, 3 plus/minus 0.3 and 3.5 plus/minus 0.5 millilitres per min) or controls (3.2 plus/minus 0.4, 3.2 plus/minus 0.3, 3.2 plus/minus 0.4 and 3.3 plus/minus 0.2 millilitres per min). Neither was there any significant variation in arterial blood pressure or heart rate throughout, in either group. These results confirm the antidiuretic effect of prolactin when endogenous vasopressin is inhibited by hypotonic fluid-loading and indicate that the effect is not caused by any change in GFR. Other possibilities include potential effects on renal reabsorptive processes and indirect effects mediated by other humoral mechanisms.
1. Morrissey, SE et al. (2001). Renal effects of recombinant prolactin in anaesthetized rats. Eur. J. Endocrinol., 145, 65-71
08 - 11 Apr 2002
British Endocrine Societies