Prolactin, diuretics and urinary electrolytes in normal subjects.

The relationship of plasma prolactin concentration and renal electrolyte excretion has been investigated in six normal male volunteers. In two studies, 80 mg frusemide were administered at 18.00 h on Day 1 and followed by dietary sodium restriction. In study A, after 38 h of sodium depletion, a second dose of frusemide was administered at 08.00 h on Day 3. In study B, after 14 h of sodium depletion, the effect of administration of 100 mg spironolactone or 45 mg prorenoate potassium (another aldosterone antagonist) at 08.00 h on Day 2 was compared with that of a placebo. After the first dose of frusemide in study A, the mean plasma prolactin concentration correlated negatively with the urinary Na and K excretion over 5 h. After 38 h sodium depletion, the plasma prolactin concentration correlated positively with urinary Na excretion following the second dose of frusemide. In study B, after Na depletion for 14 h the plasma prolactin concentration of 08.00 h on Day 2 had a positive correlation with the 24 h urinary log10 Na:K ratio following placebo administration and had negative correlations with the true urinary log10 Na:K ratio following spironolactone and prorenoate potassium administration. Neither acute Na deprivation nor the administration of single doses of frusemide, spironolactone or proprenoate potassium appeared to affect the normal circadian rhythm of plasma prolactin concentrations which remained constant for each subject throughout the 3 months covered by the investigation. The correlations of plasma prolactin concentration to renal excretion of electrolytes, with no evidence for a negative feedback control mechanism, suggest an indirect relationship between prolactin and renal function.

The effect of chlorpromazine on the secretion of immunoreactive beta-MSH and prolactin in man.

The effect of chlorpromazine (50 mg. im) on the plasma concentration of immunoreactive beta-melanocyte-stimulating hormone (beta-MSH) and prolactin was studied in 8 hospitalized subjects with non-endocrine skin disorders. Plasma beta-MSH concentrations remained unchanged over a period of 7 h in 6 subjects. In the remaining 2 subjects there was a slight increase. Plasma prolactin concentrations were greatly increased in all subjects 1 1/2-3 h after the injection and had almost returned to pre-injection levels by 7 h. This suggests that the control of beta-MSH secretion in man, unlike that of prolactin in man and MSH peptides in other mammals, is not predominantly inhibitory. The reason for this discrepancy may be that beta-MSH is not a natural MSH in man and occurs as part of the lipotropic hormone (LPH) or as a breakdown product.