ABSTRACT
Intestinal ion transport is mediated by the interaction of enterocyte function, the enteric nervous system, humoral agents, and mucosal production of carbonic anhydrase. Our purpose was to examine the effect of the carbonic anhydrase inhibitor acetazolamide and inhibition of the enteric nervous system with the topical anesthetic lidocaine on basal and prostaglandin E2-stimulated ion and water transport and transmucosal electrical potential difference. At rest, mean basal (95% confidence intervals) net ion secretion into the human proximal duodenum was: Cl- 670 (288-1052), Na+ 818 (410-1225), K+ 32 (14-51) mumol/cm/hr. Basal net water transport was 30 (14.6-45.3) ml/hr, and the potential difference (PD) was 7.0 (3.6-10.9) mV, lumen negative. Intraluminal prostaglandin E2 increased the secretion of all ions, water, and the PD. After pretreatment with acetazolamide and luminal administration of lidocaine, basal ion transport was unchanged, but the response to luminal PGE2 was inhibited. It is concluded that: (1) at rest there is a net secretion of Na+, K+, Cl-, and water by the human proximal duodenum; and (2) PGE2-stimulated water electrolyte secretion is dependent in part upon mucosal carbonic anhydrase activity and the enteric nervous system.
