Premium
Role of Calcium‐Sensing Receptor (CaSR) on Gastric Acid Secretion in Isolated Mouse Stomachs
Author(s) -
Takeuchi Koji,
Hayashi Shusaku,
Amagase Kikuko,
Aihara Eitaro
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1093.9
Subject(s) - histamine , cinacalcet , calcium sensing receptor , medicine , endocrinology , gastric acid , agonist , secretion , chemistry , somatostatin , stimulation , calcium , receptor , stomach , biology , calcium metabolism , parathyroid hormone , secondary hyperparathyroidism
In the present study, we examined the effect of cinacalcet, a CaSR agonist, on basal and stimulated gastric acid secretion in mice. Male ddY mice were used after 18 h fasting. Under urethane anesthesia, the stomach was isolated, mounted between two halves of a lucite chamber, and acid secretion was measured at pH 5.0 with 2 mM NaOH using a pH‐stat method in vitro. Histamine was added to the serosal solution. Cinacalcet was added 30 min before histamine, while CYN154806 (a somatostatin SST2 receptor antagonist) was added 30 min before cinacalcet treatment. Cinacalcet dose‐dependently and significantly suppressed the acid secretion in response to histamine, although this agent alone slightly increased the secretion. The inhibitory effect of cinacalcet was dose‐dependently reverted by pretreatment with CYN154806. Immunohistochemial study demonstrated the localization of CaSR in the stomach D cells. These results suggest that CaSR is involved in the regulatory mechanism of gastric acid secretion. It is assumed that the stimulation of CaSR negatively modulates the acid secretory response to histamine through the release of somatostatin and the activation of SST2 receptors.