J. Guillemant et S. Guillemant, MODIFICATION BY PHOSPHATE OF PTH-DEPENDENT RENAL CYCLIC-AMP RESPONSE, Hormone and Metabolic Research, 25(4), 1993, pp. 234-237
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.