The mucosal surface of the gastric antrum was covered with mucous layers, which protect the mucosa from acidpeptic injuries. The mucous layers are maintained by the Ca²⁺- regulated exocytosis from antral mucous cells. The Ca²⁺- regulated exocytosis in antral mucous cells, which is stimulated by an increase in intracellular Ca²⁺ concentration ([Ca²⁺]_i), has a characteristic feature in the secretion pattern, that is, an initial transient phase (high frequency) followed by a sustained phase (low frequency). The final process of Ca²⁺- regulated exocytosis consists of three steps, docking, ATP-dependent priming and Ca²⁺- dependent fusion. Cyclic AMP (cAMP) increases the sensitivity to Ca²⁺ in the fusion step. Moreover, cAMP, cyclic GMP (cGMP) and a decrease in intracellular Cl^- concentration accelerate the priming step and increase the number of primed granules. This enhances the frequency of initial phase. In antral mucous cells, ACh released from vagal nerve endings induces an increase in [Ca²⁺]_i which stimulates arachidonic acid (AA) accumulation leading to prostaglandin E₂ (PGE₂) production. AA directly stimulates the peroxisome proliferation activation receptor α(PPAR α), which enhances the Ca²⁺. regulated exocytosis. PGE₂, which is immediately released from cells, stimulates EP4 receptors resulting in the enhancement of Ca²⁺- regulated exocytosis via cAMP accumulation in antral mucous cells. Thus, two autocrine mechanisms via PPAR α and EP4 activated by AA modulate Ca²⁺- regulated exocytosis in ACh-stimulated antral mucous cells and maintain massive mucous secretion in the gastric antrum.