Modification by Phosphate of PTH-Dependent Renal Cyclic AMP Response

 

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Summary

The PTH response and the renal cAMP response obtained after oral administration of either tricalcium phosphate or calcium gluconolactate were compared in 12 young adult males. Each subject was studied during a control period of two hours before and during an experimental period of four hours after ingestion of a single oral dose of calcium salt. The respective dosages (1.2g of calcium plus 0.6g of phosphorus for tricalcium phosphate; 0.5 g of calcium for gluconolactate calcium) were chosen to provide similar significant (p = 0.0001) increases in serum ionized calcium (from 1.23 to 1.29 mmol/l vs from 1.23 to 1.28 mmol/l). After tricalcium phosphate a modest (10%) but significant (p<0.001) rise in serum phosphate was observed. In both series of experiments similar inhibitory effects on PTH circulating levels were obtained (from 22.6 to 12.4 pg/ml after tricalcium phosphate and from 24.1 to 10.6 pg/ml after calcium gluconolactate). After ingestion of calcium gluconolactate the renal secretion of cAMP fell from 12.68 to 8.64 nmol/l GF (p<0.001), whereas no significant alterationsof the mean values of nephrogenous cAMP were detected after ingestion of tricalcium phosphate. In accordance with the role of cAMP as a second messenger, after calcium gluconolactate we obtained a significant increase in tubular maximal reabsorption of phosphate (p<0.0001) contrasting with the absence of significant effect after tricalcium phosphate. The present results confirm that suppression of PTH secretion only depends on the rise of serum ionized calcium and suggest that additional phosphate administration could have a decoupling effect between PTH and renal cAMP secretion.