MODIFICATION BY PHOSPHATE OF PTH-DEPENDENT RENAL CYCLIC-AMP RESPONSE

The PTH response and the renal cAMP response obtained after oral admin istration of either tricalcium phosphate or calcium gluconolactate wer e compared in 12 young adult males. Each subject was studied during a control period of two hours before and during an experimental period o f four hours after ingestion of a single oral dose of calcium salt. Th e respective dosages (1.2 g of calcium plus 0.6 g of phosphorus for tr icalcium 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/1) . 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 (fr om 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 gluco nolactate the renal secretion of cAMP fell from 12.68 to 8.64 nmol/l G F (p < 0.001), whereas no significant alterations of the mean values o f nephrogenous cAMP were detected after ingestion of tricalcium phosph ate. In accordance with the role of cAMP as a second messenger, after calcium gluconolactate we obtained a significant increase in tubular m aximal reabsorption of phosphate (p < 0.0001) contrasting with the abs ence of significant effect after tricalcium phosphate. The present res ults confirm that suppression of PTH secretion only depends on the ris e of serum ionized calcium and suggest that additional phosphate admin istration could have a decoupling effect between PTH and renal cAMP se cretion.