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Calcium-sensing receptor and recovery from hypocalcaemia in thyroparathyroidectomized rats
J Huan1, G Martuseviciene, K Olgaard
1Nephrological Department P, Rigshospitalet and Herlev Hospital, University of Copenhagen, Copenhagen, Denmark.
European Journal of Clinical Investigation
|March 16, 2007
Summary
Activating the calcium-sensing receptor (CaR) with R-568 or gentamycin delayed plasma calcium recovery in rats after induced hypocalcaemia. Bone calcium sensing appears crucial for rapid minute-to-minute calcium regulation.
Area of Science:
- Physiology
- Endocrinology
- Bone Biology
Background:
- Plasma ionized calcium (p-Ca(2+)) is tightly regulated within a narrow range.
- Rapid calcium homeostasis involves flux between extracellular fluid and bone.
- The calcium-sensing receptor (CaR) is a key regulator of calcium.
Purpose of the Study:
- To investigate the role of the CaR in the rapid recovery of p-Ca(2+) following acute hypocalcaemia.
- To determine if CaR activation affects the rate of plasma calcium normalization.
Main Methods:
- Male Wistar rats underwent thyroparathyroidectomy (TPTX).
- Acute hypocalcaemia was induced using EGTA infusion.
- CaR activators (R-568, gentamycin) or vehicle were administered intravenously.
Main Results:
- EGTA infusion led to lower hypocalcaemia nadir in CaR activator-treated rats.
- Rats treated with R-568 or gentamycin showed significantly delayed p-Ca(2+) recovery.
- Vehicle-treated rats recovered basal p-Ca(2+) levels within 70 minutes, unlike CaR activator-treated rats.
Conclusions:
- CaR activators R-568 and gentamycin significantly delayed recovery from EGTA-induced hypocalcaemia in TPTX rats.
- This suggests a role for bone calcium sensing in rapid minute-to-minute p-Ca(2+) regulation.
- The findings highlight a novel mechanism in calcium homeostasis.
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