Abstract
Bicarbonate secretion from the surface epithelial cells of the gastroduodenal mucosa is an active process depending upon the tissue metabolism and plays an important role as the first line of defense in mucosal protection in collaboration with the mucus gel. This secretion is regulated by humoral and neural factors as well as endogenous prostaglandins (PGs) and is considered to be intracellularly mediated by cyclic AMP in the duodenum and by cyclic GMP in the stomach. Ca2+ also acts as an intracellular mediator in this process. This bicarbonate secretion is markedly increased in response to luminal acid, mediated by PGs and neural factors including capsaicinsensitive sensory nerves, and the impairment of this response is involved in the pathogenesis of various duodenal ulcer models induced by cysteamine, nonsteroidal antiinflammatory drugs and stress. The mechanisms underlying the mucosal protection by HCO3- secretion is two fold; One is the direct neutralization of H+ in the lumen, and the other is the establishment of a pH gradient across the mucus gel aided by the physico-chemical property of the mucus. However, the cellular mechanisms of HCO3- secretion, including the receptors, the mediators and the signal transduction pathway have been poorly understood. The establishment of a method for preparing isolated epithelial cells and the probe for HCO3- secretion in isolated cells is required to further elucidate the mechanism of HCO3- secretion.
