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J Physiol Sci ; 64(2): 129-39, 2014 Mar.
Article in English | MEDLINE | ID: mdl-24375028

ABSTRACT

Intestinal passive Mg(2+) absorption, which is vital for normal Mg(2+) homeostasis, has been shown to be regulated by luminal proton. We aimed to study the regulatory role of intestinal acid sensors in paracellular passive Mg(2+) transport. Omeprazole enhanced the expressions of acid-sensing ion channel 1a (ASIC1a), ovarian cancer G protein-coupled receptor 1 (OGR1), and transient receptor potential vanilloid 4 in Caco-2 cells. It also inhibited passive Mg(2+) transport across Caco-2 monolayers. The expression and activation of OGR1 resulted in the stimulation of passive Mg(2+) transport via phospholipase C- and protein kinase C-dependent pathways. ASIC1a activation, on the other hand, enhanced apical HCO3 (-) secretion that led, at least in part, by a Ca(2+)-dependent pathway to an inhibition of paracellular Mg(2+) absorption. Our results provided supporting evidence for the roles of OGR1 and ASIC1a in the regulation of intestinal passive Mg(2+) absorption.


Subject(s)
Acid Sensing Ion Channels/metabolism , Epithelial Cells/metabolism , Intestinal Mucosa/metabolism , Magnesium/metabolism , Receptors, G-Protein-Coupled/metabolism , Bicarbonates/metabolism , Caco-2 Cells , Calcium/metabolism , Dose-Response Relationship, Drug , Epithelial Cells/drug effects , Humans , Hydrogen-Ion Concentration , Intestinal Mucosa/drug effects , Ion Transport , Omeprazole/pharmacology , Protein Kinase C/metabolism , Time Factors , Type C Phospholipases/metabolism
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