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Ovine prolactin stimulated the 1 alpha-hydroxylase activity in isolated renal tubules and especially in primary kidney cell cultures, both prepared from vitamin D-deficient chicks. In primary chick kidney cell cultures, treated for 48 h with 1,25-dihydroxycholecalciferol (to induce the 24-hydroxylase activity) ovine prolactin, after a 1 h incubation period, stimulated the 1 alpha-hydroxylase activity without affecting the 24-hydroxylase activity. Similar results were obtained with related peptide hormones such as human growth hormone, chicken growth hormone, and human placental lactogen. These observations are discussed in relation to the possible role of these peptide hormones as modulators of 1,25-dihydroxycholecalciferol production in physiological situations of calcium stress, such as pregnancy, lactation, growth in mammals and egg laying in birds.

The effect of ovine prolactin on the renal 25-hydroxycholecalciferol-1-hydroxylase was studied in the chick. Prolactin was found to increase the activity of this enzyme in both long-term and short-term experiments. In the long term, 7 days treatment with prolactin caused a marked stimulation of the 1-hydroxylase activity, however this effect was only seen when the enzyme was assayed 2-3 hours after the final injection of prolactin. A single subcutaneous injection of prolactin was also effective in increasing the 1-hydroxylase activity, this effect was maximal at one hour and had largely disappeared 3 hours after prolactin administration.

Intestinal calcium absorption and plasma levels of 1,25-dihydroxycholecalciferol (1,25(OH)2D3) were measured in lactating and non-lacting rats and the effects of bromocriptine and exogenous prolactin treatment were evaluated. In lacting rats calcium absorption and plasma levels of parathyroid hormone, 1,25(OH)2D3 and alkaline phosphatase activity were significantly increased. Bromocriptine treatment significantly reduced the enhanced calcium absorption and levels of plasma 1,25(OH)2D3 and alkaline phosphatase but had no significant effect on plasma levels of parathyroid hormone. Prolactin administered with bromocriptine to lactating animals prevented all the changes observed with bromocriptine treatment alone. It was concluded that the increased plasma levels of prolacting during lactation lead to high plasma levels of 1,25(OH)2D3 which are responsible for the enhanced intestinal calcium absorption.

Studies in animals and tissue culture have shown the importance of prolactin and growth hormone in regulating renal 1 alpha-hydroxylase activity and plasma concentrations of 1,25-dihydroxycholecalciferol (1,25(OH)2D3). Evidence for a similar role for these hormones in man was sought by using a radioreceptor assay to measure plasma 1,25(OH)2D3 concentrations in 20 normal subjects, 12 patients receiving dialysis, 11 patients with primary hyperparathyroidism, 10 pregnant women, seven women with prolactinoma, and 14 patients with acromegaly. Circulating 1,25(OH)2D3 concentrations were appreciably raised in the patients with primary hyperparathyroidism and the pregnant women (P less than 0.001), slightly but significantly increased in the patients with prolactinoma (P less than 0.05), and greatly raised in those with acromegaly (P less than 0.001). These results suggest that prolactin and growth hormone are important regulators of renal vitamin D metabolism in the physiological conditions of pregnancy, lactation, and growth in man.

(1) Vitamin D is the precursor of an extremely potent calcium regulating hormone, 1,25(OH)2D3, which is secreted by the kidney. (2) The secretion of 1,25(OH)2D3 by the kidney is influenced by the calcium and phosphorus content of the diet, parathyroid hormone, and 1,25(OH)2D3 itself. (3)Prolactin and growth hormone are importnat regulators of vitamin D metabolism during pregnancy and growth.