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J. Biol. Chem., Vol. 276, Issue 43, 39549-39552, October 26, 2001
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From the Departments of Divalent cation receptors have recently
been identified in a wide variety of tissues and organs, yet their
exact function remains controversial. We have previously identified a
member of this receptor family in the stomach and have demonstrated
that it is localized to the parietal cell, the acid secretory cell of
the gastric gland. The activation of acid secretion has been classically defined as being regulated by two pathways: a neuronal pathway (mediated by acetylcholine) and an endocrine pathway (mediated by gastrin and histamine). Here, we identified a novel pathway modulating gastric acid secretion through the stomach calcium-sensing receptor (SCAR) located on the basolateral membrane of gastric parietal
cells. Activation of SCAR in the intact rat gastric gland by divalent
cations (Ca2+ or Mg2+) or by the potent
stimulator gadolinium (Gd3+) led to an increase in the rate
of acid secretion through the apical
H+,K+-ATPase. Gd3+ was able to
activate acid secretion through the omeprazole-sensitive H+,K+-ATPase even in the absence of the
classical stimulator histamine. In contrast, inhibition of SCAR by
reduction of extracellular cations abolished the stimulatory effect of
histamine on gastric acid secretion, providing evidence for the
regulation of the proton secretory transport protein by the receptor.
These studies present the first example of a member of the divalent
cation receptors modulating a plasma membrane transport protein and may
lead to new insights into the regulation of gastric acid secretion.
The Stomach Divalent Ion-sensing Receptor SCAR Is a Modulator of
Gastric Acid Secretion*
§¶,
,**,,,,, and
Surgery and
§ Cellular and Molecular Physiology, Yale University School
of Medicine, New Haven, Connecticut 06511 and the
** Department of General and Environmental Physiology,
University of Bari, 70125 Bari, Italy
*
This work was supported by National Institutes of Health
Grants DK50230, DK14669, and DK17433 (to J. G.) and NS12674 and
NS34569 (to L. M.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
A Feodor-Lynen fellowship of the Alexander von Humboldt
Foundation, Germany, has been awarded to C. A. W.
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