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

Citation
W. Wang et al., Parathyroid hormone is not a key hormone in the rapid minute-to-minute regulation of plasma Ca2+ homeostasis in rats, EUR J CL IN, 29(4), 1999, pp. 309-320
Citations number
38
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Journal title
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION
ISSN journal
00142972 → ACNP
Volume
29
Issue
4
Year of publication
1999
Pages
309 - 320
Database
ISI
SICI code
0014-2972(199904)29:4<309:PHINAK>2.0.ZU;2-7
Abstract
Background The role of parathyroid hormone (PTH) in the rapid minute-to-min ute regulation of plasma Ca2+ (p-Ca2+) was studied in vivo in rats. Materials and methods The rapid calcaemic response to exogenous rat PTH1-34 (16 mu g) was examined in normal rats, and the long-term calcaemic respons e was examined in parathyroidectomized (PTX) rats receiving PTH1-34 for 24 h at 0.2, 0.4 and 0.8 mu g h(-1) Acute hypocalcaemia was induced by EGTA fo r 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 additi onal doses of EGTA. Results 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 ma intaining 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 discontinui ng 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 rapi d recovery of pCa(2+) (P < 0.05) from EGTA induced hypocalcaemia. Conclusion PTH is not a key hormone in the rapid recovery of p-Ca2+ after i nduction of hypocalcaemia, but might, however, set the long-term levels of p-Ca2+ maintained by mammalian organisms. The involvement of an as yet unkn own factor in the rapid regulation of p-Ca2+ is suggested.