Parathyroid hormone is not a key hormone in the rapid minute‐to‐minute regulation of plasma Ca2+ homeostasis in rats

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Abstract
The role of parathyroid hormone (PTH) in the rapid minute-to-minute regulation of plasma Ca2+ (p-Ca2+) was studied in vivo in rats. The rapid calcaemic response to exogenous rat PTH1–34 (16 μg) was examined in normal rats, and the long-term calcaemic response was examined in parathyroidectomized (PTX) rats receiving PTH1–34 for 24 h at 0.2, 0.4 and 0.8 μg h−1. Acute hypocalcaemia was induced by EGTA for 30 min, and then the rapid recovery of p-Ca2+ was studied for 130 min in normal rats, 24 h after PTX and in PTX rats infused with exogenous rat PTH1–34. The dynamics of the rapid recovery of p-Ca2+ was studied at two additional doses of EGTA. No rapid calcaemic response was observed in the first 60 min after administration of PTH and no hypocalcaemia was seen for 2 h after acute PTX. This slow effect of PTH suggests that PTH might not be responsible for maintaining the stable p-Ca2+ on a rapid minute-to-minute basis. EGTA induced acute hypocalcaemia in both normal and PTX rats (P < 0.01). In both groups a rapid and similar increase in p-Ca2+ took place 10 min after discontinuing EGTA (P < 0.05). Within 60 min, p-Ca2+ increased further, independently of the presence of PTH. Infusion of PTH to PTX rats did not affect the rapid recovery of p-Ca2+ (P < 0.05) from EGTA induced hypocalcaemia. PTH is not a key hormone in the rapid recovery of p-Ca2+ after induction of hypocalcaemia, but might, however, set the long-term levels of p-Ca2+ maintained by mammalian organisms. The involvement of an as yet unknown factor in the rapid regulation of p-Ca2+ is suggested.