Abstract

The physiological significance of parathyroid hormone in the regulation of bone resorption and serum calcium was established by the work of Collip [1] and others in the 1920′s. Early investigators also recognized that the kidney was important in parathyroid hormone action. Greenwald and Gross discovered that parathyroidectomy caused a rapid fall in the rate of excretion of phosphate into the urine, and that injection of parathyroid extract caused urine phosphate excretion to rise [2]. The effect on phosphate excretion was so rapid as to lead some to believe that regulation of calcium was mediated through the hormone's phosphaturic influence on the kidney [3]. Physiologists later proved that parathyroid hormone acts directly on bone as well as on kidney. The kidney, moreover, has been established as an important organ mediator for regulation of calcium in the extracellular fluid. The role of the kidney as an effector of parathyroid action, however, is due to its influence on calcium, not phosphate excretion. The subsequent discovery [4] of calcitonin, another hormone involved in regulating calcium metabolism, led to the finding that it too influences renal physiology. It causes an increase in urinary excretion of sodium, phosphate and calcium. Moreover, specific hormone receptors for calcitonin in the nephron have been identified. Nevertheless, it is still unclear whether these renal effects of calcitonin are important in its physiological control of calcium. In this paper we discuss the physiological actions 1 of parathyroid hormone and calcitonin on the kidney.

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