Laboratory Investigation

Kidney International (1985) 27, 394–400; doi:10.1038/ki.1985.22

Modulation by calcitonin of magnesium and calcium urinary excretion in the rat

Antonio Di Stefano1, Jean-Marc Elalouf1, Jean-Michel Garel1 and Christian de Rouffignac1

1Laboratoire de Physiologie Physico-Chimique, Département de Biologie, Centre d'Etudes Nucléaires de Saclay, and Groupe "Hormones du calcium et Développement," Université Pierre et Marie Curie, Paris, France

Correspondence: Dr C de Rouffignac, DB/LPPC, C.E.N. Saclay, 91191 Gif-sur-Yvette, France

Received 5 July 1983; Revised 21 May 1984.

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Abstract

Modulation by calcitonin of magnesium and calcium urinary excretion in the rat. We evaluated the effects of human calcitonin (hCT) on electrolyte excretion in hormone-deprived rats, that is, in the absence of endogenous parathyroid hormone, antidiuretic hormone, thyrocalcitonin and glucagon, the effects of which might have interfered with those of exogenous calcitonin. Plasma hCT levels, measured by radioimmunoassay, varied from 0 to 32 ng/ml. In these rats, hCT decreased magnesium (Mg) and calcium (Ca) excretion in a dose-dependent fashion. Maximal decreases were observed for hCT plasma concentrations comprised between 3 and 5 ng/ml, and persisted at the highest doses. Sodium, potassium, water, and total solute excretions were constant in the calcitonin concentration range explored. The same was observed for phosphate, except that slight but significant phosphaturia was elicited by the highest doses. Calcium and phosphate infusions to attenuate the fall in plasma Ca and phosphate concentration subsequent to hCT infusion, did not alter the hormonal effect on Ca and Mg excretion. hCT can therefore directly modulate Mg and Ca reabsorption by the kidney at plasma concentrations within the physiological range. The maximal effects on Mg and Ca reabsorption were obtained at plasma concentrations which are generally reached after maximal stimulation of endogenous calcitonin secretion. It is suggested that in rats, endogenous secretion of calcitonin stimulates Ca and Mg renal reabsorption without modification of sodium and phosphate excretion.

Modulation de l'excrétion urinaire de magnesium et calcium par la calcitonine chez le rat. Les effets de la calcitonine humaine sur l'excrétion des électrolytes ont été étudiés chez le rat anhormonal, c'est-à-dire, en l'absence des hormones endogènes (hormone parathyroïdienne, hormone antidiurétique, calcitonine et glucagon) dont les effets auraient pu interférer avec ceux de la calcitonine exogène. La concentration plasmatique de calcitonine, mesurée par radioimmunologie, était comprise entre 0 et 32 ng/ml. Chez ces rats, l'excrétion du magnesium (Mg) et celle du calcium (Ca) était fonction de la concentration de calcitonine circulante. Ces excrétions atteignient leur valeur minimale pour des concentrations plasmatiques de calcitonin comprises entre 3 et 5 ng/ml, et se maintenaient à ce niveau aux concentrations plus élevées. L'excrétion du sodium, du potassium, du phosphate, de l'eau et des solutés totaux était constante et indépendante de la concentration de calcitonine circulante. Cependant aux concentrations plasmatiques les plus élevées, une phosphaturie modérée mais significative est apparue. La calcitonine peut donc moduler la réabsorption rénale de Mg et Ca quand son taux circulant varie dans les limites physiologiques. Les effets maximum sur la réabsorption de Mg et Ca furent obtenus pour des concentrations plasmatiques généralement atteintes après stimulation maximale de la sécrétion de calcitonine endogène. Il est suggéré que la sécrétion de calcitonine endogène induit chez le rat une augmentation de la réabsorption rénale du magnésium et du calcium sans modification de l'excrétion du sodium et du phosphate.

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