Studies on molecular mechanisms of exocytosis

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It was suggested that nitric oxide inhibits exocytosis of insulin in pancreatic B cells, by inhibiting ATP synthesis which results in prohibition of closure of KィイD2ATPィエD2 channels due to inhibition of depolarization. Photodynamic action in SALPc-loaded rat peritoneal mast cells inhibited compound 48/80-induced exocytosis of secretory granules, indicating that singlet oxygen produced by photodynamic action may interfere with exocytotic process. It was demonstrated that, in rat pancreatic B cells, NaィイD1+ィエD1/CaィイD12+ィエD1 exchanger may contribute to glucose-induced exocytotic mechanisms. It was suggested that there were different CaィイD12+ィエD1 signalling mechanisms in acinar cells and in myoepithelial cells of guinea-pig lachrymal gland, which can be triggered with different agonists. In rat adrenal chromaffin cells, cholinergic agonist-induced exocytosis correlates with the development of both intracellular signalling mechanisms and innervation, and nicotinic mechanisms seemed to precede the appearance of muscarinic mechanisms. Carbachol-induced exocytosis is inhibited by oxidative stress in pancreatic acinar cell and [CaィイD12+ィエD1], signalling process is also disturbed the stress. Inhibition by Substance P of nicotine-induced catecholamine secretion in rat chromaffin cells is noncompetitive, suggesting that substance P inhibit the function of probably NaィイD1+ィエD1 channel domain of nicotinic receptor. Neuronal death of rat cortex can be due to disturbance of [CaィイD12+ィエD1]ィイD2iィエD2 homeostasis. In mouse ileal crypt cells, activation of G-protein and ATP can induced [CaィイD12+ィエD1]ィイD2iィエD2, elevation. All these results indicate that intracellular CaィイD12+ィエD1 plays important roles in both physiological and pathological process of various cells.