Reduction in Jejunal Fluid Absorption In vivo through Distension and Cholinergic Stimulation Not Attributable to Enterocyte Secretion

Jejunal fluid absorption in vivo was reduced by distension and by hydrostatic pressure and further declined on adding E. coli STa enterotoxin but no net fluid secretion was detected. Luminal atropine reduced pressure mediated reductions in fluid absorption to normal values but intravenous hexamethonium was without effect. A neural component to inhibition of absorption by pressure (though not stretch) may be mediated by axon reflexes within cholinergic neurons.Perfusion of cholinergic compounds also reduced net fluid absorption but did not cause secretion. In order to show that these actions were not secretory processes stimulated by cholinergic compounds that offset normal rates of absorption, these compounds were tested for their ability to cause net secretion in loops that were perfused with solutions in which choline substituted for sodium ion. In addition, these perfusates additionally contained E. coli STa enterotoxin or EIPA (ethyl-isopropyl-amiloride) to minimize absorption.In these circumstances, where it might be expected to do so if it were acting through a secretory rather than an absorptive mechanism, carbachol did not cause net fluid secretion. Cholinergic stimulation and pressure induced distension are thought to reduce net fluid absorption through inducing secretion but are found only to reduce fluid absorption.In conclusion, distension and cholinergic stimulation of the small intestine are two further circumstances in which fluid secretion is assumed to explain their action on fluid movement, as required by the enterocyte secretion model of secretion but, which like STa enterotoxin, instead are only able to reduce fluid absorption. This casts further doubt on the widespread validity of the enterocyte secretion model for fluid appearance in the lumen in diarrhoeal diseases.