Effects of
1,25(OH)2D3 or 24,25(
OH)2D3 on plasma PTH were examined following induced
hypocalcemia with
EGTA.
EGTA infusions caused an elevation of plasma PTH within 10 min. Sixty min after the start of
EGTA infusions,
1,25(OH)2D3 or 24,25(
OH)2D3 were IV administered. Transient (within 5 min) elevations in plasma PTH were observed in two of five animals following the administration of
1,25(OH)2D3 or of 24,25(
OH)2D3. Neither secosterol had an effect on the induced elevations in plasma PTH during the remaining 60 min of the
EGTA infusions. Twenty-two hr following 24,25(
OH)2D3 administration, plasma PTH, ionized and total
calcium,
inorganic phosphate, and
magnesium were normal, while plasma 24,25(
OH)2D was elevated. The plasma PTH response to
EGTA-induced
hypocalcemia was not significantly altered from that observed prior to the administration of 24,25(
OH)2D3. Animals, which were IV injected with
1,25(OH)2D3 received the same amount IM 60 min later. Twenty-two h following IM
1,25(OH)2D3, plasma 1,25(
OH)2D, ionized and total
calcium, and plasma
inorganic phosphate were elevated. Plasma PTH and
magnesium were lowered. The PTH response to
EGTA-induced
hypocalcemia was significantly reduced in these animals. A similar reduction in the PTH response to induced
hypocalcemia was observed in animals receiving 7 hr IV infusions of
calcium chloride. The findings suggest that the blunted response was, in part, the consequence of the preceding
hypercalcemia. These results indicate that
1,25(OH)2D3 does not directly regulate plasma PTH secretion and that 24,25(
OH)2D3 has no effect on plasma PTH during induced
hypocalcemia in the bovine species.