Effect of ACTH, α-MSH, and β-Lipotropin on Calcium and Phosphorus Metabolism in the Rabbit

Abstract

Studies were undertaken to investigate the effects of synthetic 1-24 adrenocorticotropin (ACTH), bovine alpha melanocyte-stimulating hormone (alpha-MSH), and ovine beta lipotropin (beta-LPH) on plasma calcium and phosphate in rabbits. Equimolar concentrations of these hormones were infused intravenously in intact and thyroidectomized animals. In addition, ACTH was similarly administered to adrenalectomized rabbits. ACTH, alpha-MSH, and beta-LPH all lowered plasma calcium and raised plasma phosphate. These changes were not prevented by prior thyroidectomy. ACTH was equally effective in inducing hypocalcemia and hyperphosphatemia in the absence of the adrenal glands, while adrenalectomy alone raised plasma calcium. From these findings we have concluded that 1) ACTH, alpha-MSH, and betaLPH affect phosphate as well as calcium metabolism; 2) these hormones do not act by releasing calcitonin; and 3) ACTH exerts its hypocalcemic-hyperphosphatemic effect, at least in part, independently of its trophic action on the adrenal glands.

In-vivo hypocalcaemic, hypophosphataemic and hyperlipaemic activities in the common peptide sequence of adrenocorticotrophin, melanocyte-stimulating hormone and lipotrophin

“…Six years later, Akgün & Rudman (1969) corroborated this work and showed that a-MSH gave a similar result. More recently, Gildersleeve et al (1975) injected rabbits with these hormones (the molecules of which shared the same peptide sequence); they not only confirmed the presence of hypocalcaemia but also revealed the presence of hypophosphataemia. Chrétien et al (1973) also found hypocalcaemia with LPH but observed normal blood calcium in previously thyroidectomized rabbits injected with this hormone.…”

“…which they attributed to the release of calcitonin from the thyroid gland. However, Gildersleeve, Pearson, Baghdiantz & Foster (1975) were unable to show the mediation of the thyroid gland in the hypocalcaemia occurring after administration of ACTH, a-MSH and ß-LPH. Moreover, their findings indicate that ACTH does not induce hypocalcaemia through stimulating the secretory activity of the adrenal cortex.…”