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P2Y Purinoceptor Mediates Ca2+ Signaling in Duodenocytes and Involves Duodenal Mucosal Bicarbonate Secretion

Purinergic receptors have been identified in most epithelial tissues, including gastrointestinal tract. Although the role of P2Y purinoceptors and their signaling in the intestinal epithelial Cl− secretion have been studied extensively, little is known about the expression and function of P2Y purinoceptors in the duodenum, especially their role in duodenal mucosal bicarbonate secretion (DMBS). Duodenal mucosae from C57BL mice were stripped of seromuscular layers and mounted in Ussing chambers. Both short‐circuit current (Isc) and HCO3 − secretion were measured in these tissues. Acid‐stimulated DMBS was also measured in vivo. Cytoplasmic free Ca2+ ([Ca2+]cyt) was determined by digital imaging in SCBN cells, a duodenal epithelial cell line. UTP (10 μM) significantly induced duodenal Isc and HCO3− secretion, which were abolished by the pretreatment of the tissues with either suramin (300 μM), a P2 receptor antagonist or 2‐APB (100 μM), a store‐operated channel inhibitor. Acidstimulated DMBS in vivo was significantly blocked by suramin (1 mM). Both ATP and UTP at 10 μM raised comparable [Ca2+]cyt in SCBN cell in the presence or the absence of extracellular Ca2+, which were prevented by the pretreatment with either suramin or 2‐APB. However, ADP at 10 μM raised smaller [Ca2+]cyt in these cells. These results suggest that activation of P2Y purinoceptors in the duodenal epithelium may increase [Ca2+]cyt by inducing intracellular Ca2+ release and extracellular Ca2+ entry via SOC, and thereby stimulate duodenal Cl− and HCO3− secretion (Supported by Cystic Fibrosis Foundation).