Nifedipine has been shown to lower urinary calcium in "essential" hypercalciuria. However, the mechanism(s) by which this action takes place is completely unknown. This study describes the effect of nifedipine on some calcium-controlling hormones in essential hypercalciuria. Nifedipine (20 mg/day) was administered to ten essential hypercalciuric patients, and urinary PgE2, plasma bicyclic PgE2, 1,25 vitamin D3, and PTH were assayed before and after drug administration. Nifedipine promoted a significant fall in urinary calcium (352.1±87.67 SD vs. 231.2±74.62 mg/24 hr; t=7.35, p<.0001) and PgE2 (343.92±42.71 vs. 245.03±35.41 SD ng/24 hr; t=6.18, p<.0002), as well as in plasma bicyclic PgE2 (310.00±30.91 vs. 200.00±31.62 SD pg/ml; t=9.86, p<.0001) and 1,25 (OH)2 vitamin D3 (32.77±3.23 vs. 26.94±2.94 SD pg/ml; t=6.53, p<.0001), while PTH remained unaltered (18.50±3.63 vs. 19.50±4.09 SD ng/ml; t=0.85, p, ns). Urinary calcium and PgE2 correlated positively before (r=0.81, p<.005) but not after treatment. The fall in urinary PgE2 brought about by nifedipine seems to be due to an inhibition of PgE2 synthesis, since the absolute decrements in both urinary PgE2 and plasma PgE2 metabolites were positively correlated (r=0.79, p<.007). No correlation was found between the absolute decrements of plasma bicyclic PgE2 and 1,25 (OH)2 vitamin D3. These data seem to suggest that the fall in urinary calcium brought about by nifedipine is insome way related to PgE2 synthesis inhibition and to uncoupling of 1,25 (OH)2 vitamin D3 and PTH action. © 1990 Kluwer Academic Publishers.
Effect of nifedipine on urinary excretion of calcium and calcium-controlling hormones in essential hypercalciuria
CALO', LORENZO
;D'ANGELO A;GIANNINI S;BORSATTI A.
1990
Abstract
Nifedipine has been shown to lower urinary calcium in "essential" hypercalciuria. However, the mechanism(s) by which this action takes place is completely unknown. This study describes the effect of nifedipine on some calcium-controlling hormones in essential hypercalciuria. Nifedipine (20 mg/day) was administered to ten essential hypercalciuric patients, and urinary PgE2, plasma bicyclic PgE2, 1,25 vitamin D3, and PTH were assayed before and after drug administration. Nifedipine promoted a significant fall in urinary calcium (352.1±87.67 SD vs. 231.2±74.62 mg/24 hr; t=7.35, p<.0001) and PgE2 (343.92±42.71 vs. 245.03±35.41 SD ng/24 hr; t=6.18, p<.0002), as well as in plasma bicyclic PgE2 (310.00±30.91 vs. 200.00±31.62 SD pg/ml; t=9.86, p<.0001) and 1,25 (OH)2 vitamin D3 (32.77±3.23 vs. 26.94±2.94 SD pg/ml; t=6.53, p<.0001), while PTH remained unaltered (18.50±3.63 vs. 19.50±4.09 SD ng/ml; t=0.85, p, ns). Urinary calcium and PgE2 correlated positively before (r=0.81, p<.005) but not after treatment. The fall in urinary PgE2 brought about by nifedipine seems to be due to an inhibition of PgE2 synthesis, since the absolute decrements in both urinary PgE2 and plasma PgE2 metabolites were positively correlated (r=0.79, p<.007). No correlation was found between the absolute decrements of plasma bicyclic PgE2 and 1,25 (OH)2 vitamin D3. These data seem to suggest that the fall in urinary calcium brought about by nifedipine is insome way related to PgE2 synthesis inhibition and to uncoupling of 1,25 (OH)2 vitamin D3 and PTH action. © 1990 Kluwer Academic Publishers.
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