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Calcium‐sensing receptor and recovery from hypocalcaemia in thyroparathyroidectomized rats
Author(s) -
Huan J.,
Martuseviciene G.,
Olgaard K.,
Lewin E.
Publication year - 2007
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.2007.01770.x
Subject(s) - hypocalcaemia , calcium , endocrinology , receptor , calcium sensing receptor , medicine , chemistry , calcium metabolism
Background Plasma ionized calcium (p‐Ca 2+ ) is kept within a very narrow range and deviations are rapidly corrected by flux of Ca 2+ between extracellular fluid and the labile calcium pool at the quiescent bone surface. The calcium sensing at the bone surface represents a physiological interesting model for the rapid minute‐to‐minute regulation of p‐Ca 2+ . Our aim was to study whether the calcium‐sensing receptor (CaR) has a role in the rapid recovery of p‐Ca 2+ from acute induced hypocalcaemia. Material and methods Male Wistar rats were thyroparathyroidectomized (TPTX). Acute hypocalcaemia in the animals was induced by infusion of EGTA (40–50 m m EGTA, 3·0 mL h −1 for 30 min). Thereafter the recovery of p‐Ca 2+ was followed. Vehicle or the CaR activators, R‐568 (2 mg as a bolus twice) or gentamycin were administrated intravenously. Results EGTA infusion resulted in significantly lower nadir of hypocalcaemia in R‐568‐ or gentamycin‐treated rats compared to vehicle‐treated rats ( P < 0·01). During recovery phase p‐Ca 2+ remained significantly lower in R‐568 rats ( P < 0·001). As such p‐Ca 2+ levels recovered to basal levels in the vehicle group within 70 min after stopping EGTA, while R‐568 or gentamycin rats remained significantly hypocalcaemic. Conclusions The CaR activators R‐568 and gentamycin, both significantly delayed the recovery of p‐Ca 2+ from acute EGTA‐induced hypocalcaemia in TPTX rats. This novel finding suggests the existence of calcium sensing by bone of importance for the rapid minute‐to‐minute regulation of p‐Ca 2+ .