Effect of Parathyroid Hormone, Vitamin D and Calcitonin on Aluminum Kinetics

摘要

Current methods of tissue aluminum analysis have been simplified by replacing an EDTA extraction with a nitric acid digestion. Both procedures have been confirmed by the use of plasma emission spectrometry and applied to studies of aluminum metabolism. Animals fed normal laboratory diets demonstrate appreciable aluminum content in numerous tissues which increased with time. The addition of aluminum to the diet results in a dose and time related accumulation of aluminum in most tissue studied. The chemical form of oral aluminum is also an important determinant of tissue aluminum burdens especially in uremia. In addition to exogenous PTH, maneuvers to stimulate endogenous PTH secretion such as vitamin D defficiency and uremia also enhance specific tissue aluminum burdens. Supporting this concept is a decline in specific tissue aluminum burdens following PTH withdrawal in both animals and man. The mechanism by which PTH effects aluminum metabolism is not mediated by hypercalcemia or 1,25(OH)2-D3 production. Suprisingly 25(OH)-D3 has specific effects on aluminum metabolism also independent of hypercalcemia. In addition, aluminum seems to have an effect on either decreasing PTH release and/or altering end organ response to PTH. Finally, PTH mediated increases in brain aluminum content in both the rat and rabbit do not result in specific histologic changes.