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J Biol Chem, Vol. 273, Issue 31, 19579-19586, July 31, 1998
From the Endocrine-Hypertension Division, Department of Medicine,
Brigham and Women's Hospital, Boston, Massachusetts 02115
The calcium-sensing receptor (CaR) is activated
by small changes in extracellular calcium
[Ca2+]o) in the
physiological range, allowing the parathyroid gland to regulate serum
[Ca2+]o; however, the CaR is also
distributed in a number of other tissues where it may sense other
endogenous agonists and modulators. CaR agonists are polycationic
molecules, and charged residues in the extracellular domain of the CaR
appear critical for receptor activation through electrostatic
interactions, suggesting that ionic strength could modulate CaR
activation by polycationic agonists. Changes in the concentration of
external NaCl potently altered the activation of the CaR by external
Ca2+ and spermine. Ionic strength had an inverse effect on
the sensitivity of CaR to its agonists, with lowering of ionic strength
rendering the receptor more sensitive to activation by
[Ca2+]o and raising of ionic
strength producing the converse effect. Effects of osmolality could not
account for the modulation seen with changes in NaCl. Other salts,
which differed in the cationic or anionic species, showed shifts in the
activation of the CaR by [Ca2+]o
similar to that elicited by NaCl. Parathyroid cells were potently
modulated by ionic strength, with addition of 40 mM NaCl
shifting the EC50 for
[Ca2+]o inhibition of parathyroid
hormone by at least 0.5 mM. Several CaR-expressing tissues,
including regions of the brain such as the subfornical organ and
hypothalamus, could potentially use the CaR as a sensor for ionic
strength and NaCl. The Journal guidelines state that the summary should
be no longer than 200 words.
Sodium and Ionic Strength Sensing by the Calcium Receptor
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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