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Articles in PresS, published online ahead of print March 20, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00500.2001
Submitted on November 27, 2001
Accepted on March 17, 2002
1 Department of Cellular & Molecular Physiology, Yale University, New Haven, CT, USA
2 Department of Cellular & Molecular Physiology, Yale University, New Haven, CT, USA; Department of Surgery, Yale University, New Haven, CT, USA
* To whom correspondence should be addressed. E-mail: sam.cheng{at}yale.edu.
The calcium-sensing receptor (CaSR) is activated by extracellular calcium (Ca2+o) and mediates many of the known effects of extracellular divalent minerals on body cells. Both surface and crypt cells express CaSR transcripts and protein on both apical and basolateral surfaces. Raising Ca2+o elicited increases in Ca2+i in both surface and crypt cells with an EC50 of 2 mM. The Ca2+o-induced increase in Ca2+i was associated with increases in IP3 and eliminated by an inhibitor of phosphatidylinositol-phospholipase C (U-73122) as well as by thapsigargin. Other CaSR agonists, Gd3+ and neomycin, mimicked these Ca2+o-induced responses. Both luminal and bath Ca2+o, Gd3+ and neomycin induced increases in Ca2+i in isolated perfused crypts. The stimulatory effect of forskolin on net fluid secretion in perfused crypt was abolished by increasing Ca2+o in either luminal or bath perfusates. Thus, both apical and basolateral CaSR on crypt cells are functional and provide pathways modulating net intestinal fluid transport that may have important implications for the prevention and treatment of certain diarrheal diseases associated with elevated cAMP.
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