Gastric mucosal protective mechanisms: roles of epithelial bicarbonate and mucus secretions

Abstract

Secretion of HCO3 (amounting to 2-10% of maximum H+ secretion) in conjunction with the adherent mucus gel layer (functioning as a mixing barrier) protects gastric mucosa from luminal acid by a process of surface neutralization. Gastric HCO3 secretion is augmented by cholinergic agonists, prostaglandins and low luminal pH. Ulcerogens attenuate HCO3 secretion although passive diffusion of alkali consequent upon an increase in mucosal permeability may mask these inhibitory actions. Studies in vitro indicate that HCO3 transport in the stomach is dependent on oxidative metabolism, carbonic anhydrase activity and involves a CL exchange mechanism. Mucus, synthesized and released from epithelial cells, adheres to the mucosal surface as a thin (less than 80 microns in rat) but continuous gel layer. Prostaglandins and carbachol induced release of preformed mucus and thereby increase thickness, whereas acute exposure to ulcerogens has little effect on overall dimensions of the surface mucus layer. Measurements of pH gradients adjacent to gastric mucosa indicate that the disposal of luminal H+ occurs by extracellular neutralization. However, the fall in pH at the apical cell membrane when luminal pH is low (pH 1.5) suggests that while a mucus-bicarbonate barrier comprises the first line of mucosal defence, other factors are involved in the overall process of mucosal protection in the stomach.