PARATHYROIDECTOMY ABOLISHES THE INCREASE OF RENAL 25-HYDROXYVITAMIN D-1-ALPHA-HYDROXYLASE IN LACTATING RATS

Serum ionized calcium (Ca), but not inorganic phosphorus or immunoreac tive parathyroid hormone, negatively correlates with renal 25-hydroxyv itamin D-1alpha-hydroxylase (1alpha-hydroxylase) and serum 1,25-dihydr oxyvitamin D in intact lactating rats. The present study tested the hy pothesis that the presumed stimulation of renal 1alpha-hydroxylase by hypocalcemia requires the presence of intact parathyroid glands. Lacta ting and nonlactating rats were surgically parathyroidectomized (PTX) or sham-operated (sham) at 9-10 days of lactation. Later (24 h) the ra ts were bled, nephrectomized, and killed. In lactating PTX rats, serum ionized Ca decreased to 50% of the level of sham rats, and serum 1,25 -dihydroxyvitamin D fell to 37 +/- 5.0 pg/ml compared with 82 +/-13.0 pg/ml for sham lactating rats but was still 2.5 times the value for no nlactating PTX rats (15 +/- 0.8 pg/ml). In contrast to the still eleva ted serum 1,25-dihydroxyvitamin D concentration in lactating PTX rats, renal 1alpha-hydroxylase was suppressed to the same low level as in n onlactating PTX rats, suggesting the existence of extrarenal synthesis of 1,25-dihydroxyvitamin D in lactation. A curvilinear relationship w as revealed between serum ionized Ca and renal 1alpha-hydroxylase in s ham lactating and nonlactating rats (r2 = 0.71, P < 0.000 1). However, in PTX rats, decreasing ionized Ca did not lead to any increase in 1a lpha-hydroxylase above the low baseline values seen at ionized Ca conc entrations between 1.3 and 1.5 mM. We therefore conclude that intact p arathyroid glands are required for hypocalcemia to activate renal 1alp ha-hydroxylase in female rats.