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Acid-sensing protective mechanisms of duodenum

100%

Kaunitz J. D., Akiba Y.

Journal of Physiology and Pharmacology. Supplement

2003

tom 54

nr 4

19-26

The proximal duodenal mucosa, exposed to frequent pulses of gastric acid, is functionally "leaky", increasing the importance of defense mechanisms such as the mucus gel layer, cellular acid/base transporters, bicarbonate secretion, and mucosal blood flow. Our laboratory has used a unique in vitro perfused microscopic system to measure thickness of the adherent mucus gel (MGT), intracellular pH (pHi), bicarbonate secretion, and mucosal blood flow in anesthetized rats. Exposure to pulses of luminal acid, mimicking the rapid physiologic shifts of luminal pH, increases MGT and blood flow, and induces cellular bicarbonate loading, the latter followed by augmented bicarbonate secretion. The mechanism by which the epithelium senses luminal acid includes capsazepine-inhibitable vanilloid receptors, presumably similar to the vanilloid receptor TPVR-1. CFTR, the cAMP-regulated anion channel mutated in the disease cystic fibrosis, plays an essential role in duodenal bicarbonate secretion. Our data are consistent with the hypothesis that cellular bicarbonate loading is an important means of preserving epithelial pHi during luminal acid challenge. Increased MGT may damp rapid shifts of luminal pH. Enhanced mucosal blood flow plays a significant role in the removal of back-diffusing acid. These neurally coordinated systems act coherently to defend the vulnerable duodenal epithelial cells from concentrated gastric acid.

Solute diffusion through stripped mouse duodenum

61%

Takeuchi T., Ham M., Mizumori M., Guth P. H., Engel E., Kaunitz J. D., Akiba Y.

Journal of Physiology and Pharmacology

2007

tom 58

nr 4

We measured villous cell intracellular pH (pHi) and solute diffusion between the bathing media and the epithelial cells in stripped, chambered mouse duodenum. Apical perfusion of a high CO2 solution rapidly acidified the upper villous cells with recovery after its removal. Apical zoniporide (ZP) enhanced CO2-induced acidification. Serosal ZP, dimethylamiloride (DMA) or stilbene anion transport inhibitors failed to alter CO2-induced acidification, whereas serosal high CO2 buffer acidified the upper villous cells. Serosal 5-hydroxytryptamine rapidly acidified the upper villous cells. All serosally-perfused fluorescent compounds stained the crypt area, but not the villi or villous cells. In contrast, intravenous carboxyfluorescein quickly diffused into the interstitial space of the entire mucosa, and mucosally perfused fluorescent compound rapidly penetrated the epithelial cell layer. In muscle-stripped duodenum mounted in a small-aperture perfusion chamber, serosal solutes can readily diffuse only to the crypt cell region, whereas access to the villous epithelial cells is diffusion-limited. In contrast, rapid villous cell responses to serosally applied solutes are best explained by neural reflexes. Limited viability of the villous cells and impaired structural stability of the villi further limit long-term, villous cell functional studies of mucosal preparations mounted in small aperture diffusion chambers.

Ograniczanie wyników

1 Journal of Physiology and Pharmacology

1 Journal of Physiology and Pharmacology. Supplement

2 Akiba Y.

2 Kaunitz J. D.

1 Engel E.

1 Guth P. H.

1 Ham M.

1 Mizumori M.

1 Takeuchi T.

1 2007

1 2003

Wyniki wyszukiwania

Acid-sensing protective mechanisms of duodenum

Solute diffusion through stripped mouse duodenum