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.
Calcium - Phosphate - Parathyroid Hormone - Cyclic AMP
