Gastroduodenal mucosal defense: an integrated protective response.

Purpose Of Review: The remarkable resistance of the mucosal lining the upper gastrointestinal tract to concentrated gastric acid remains one of the biggest unsolved mysteries of upper gastrointestinal physiology. Even with the discovery of the involvement of Helicobacter pylori in gastroduodenal injury, the mechanism by which the organism causes injury remains unresolved. In the past year, there have been striking findings regarding trefoil peptides, the protective effect of regulatory peptides such as adrenomedullin, and the influence of H.

Mechanism of augmented duodenal HCO(3)(-) secretion after elevation of luminal CO(2).

The proximal duodenum is exposed to extreme elevations of P(CO(2)) because of the continuous mixture of secreted HCO(3)(-) with gastric acid. These elevations (up to 80 kPa) are likely to place the mucosal cells under severe acid stress. Furthermore, we hypothesized that, unlike most other cells, the principal source of CO(2) for duodenal epithelial cells is from the lumen.

NHE3 inhibition activates duodenal bicarbonate secretion in the rat.

We examined the effect of inhibition of Na+/H+ exchange (NHE) on duodenal bicarbonate secretion (DBS) in rats to further understand DBS regulation. DBS was measured by using the pH-stat method and by using CO2-sensitive electrodes. 5-(N,N-dimethyl)-amiloride (50 microM; DMA), a concentration that selectively inhibits the NHE isoforms NHE1 and NHE2, but not NHE3, did not affect DBS.