Several studies have shown an increase in urinary calcium excretion in response to a calcium load. However, because of the inverse changes in PTH levels with a calcium load, the effect of changes in serum calcium per se on its own excretion is unclear in humans. In this study we used a PTH clamp protocol to further characterize calcium-regulated renal calcium and magnesium handling and the relationship of the former to sodium excretion. Eight normal male subjects were evaluated using a calcium clearance protocol with graded calcium infusions under a PTH clamp while in balance during a high and then during a low sodium diet. The curves describing calcium and magnesium excretion as a function of serum ionized calcium on the high sodium diet were best fitted by sigmoidal functions, with midpoints (the levels of calcium resulting in half-maximal increases in urinary cation excretion) of 1.51 and 1.49 mmol/L, respectively. The curve describing urinary sodium as a function of serum calcium was also sigmoidal on the high sodium diet, with a midpoint of 1.55 mmol/L. Our data taken in conjunction with those of previous studies evaluating sodium and calcium excretion in diseases characterized by inactivating or activating mutations in the calcium receptor, are consistent with the hypothesis that PTH-independent, calcium-dependent changes in renal calcium, magnesium, and sodium handling may be mediated at least in part by this receptor, which is known to be located in the loop of Henle.
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