B. Lobaugh et al., PARATHYROIDECTOMY ABOLISHES THE INCREASE OF RENAL 25-HYDROXYVITAMIN D-1-ALPHA-HYDROXYLASE IN LACTATING RATS, The American journal of physiology, 264(6), 1993, pp. 981-985
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.