The short-circuit current (Isc), potential difference (PD), tissue conductance (Gt), and Na and Cl fluxes in the short-circuit state across rat ileum were studied in Ussing chambers using a variety of bathing solutions. In Ringer solution, Isc exceeded net Na absorption and net Cl secretion occurred. Addition of 10 mM glucose increased Isc, PD, Gt, and net Na absorption, which accounts for 70% of the increase in Isc. Removal of HCO3 from Ringer solution did not alter any parameters but increased net Cl secretion due to a decrease in mucosal-to-serosal Cl flux. Reduction by 50% of the [Cl] in HCO3-free solution decreased the net Cl secretion to the level in Ringer solution and increased net Na absorption. Removal of Cl decreased Isc to the value of the net Na absorption and decreased the Na influx across the mucosal membrane by 39%. Isc and PD were near zero and net Cl absorption was observed in a Na-free solution. These results are consistent with the transport mechanism that consists of 1) an electrogenic Na absorptive process that accounts for the Isc, 2) a neutral NaCl-coupled secretory process, and 3) a system by which HCO3- secretion exchanges for Cl- absorption.
1. The electrical potential difference, short-circuit current, tissue conductance, and fluxes of sodium and chloride were measured in rat small intestine in an in vitro chamber preparation in the presence and absence of 100 mM-mannitol on either the mucosal or serosal surface. 2. Mucosal mannitol generally decreased potential difference, short-circuit current, and tissue conductance while serosal mannitol increased the electrical variables. 3. Mucosal mannitol decreased unidirectional movement of sodium and chloride but did not change the net transport of these ions. The change in short-circuit current was therefore ascribed to changes in fluxes of ions other than sodium and chloride. 4. Serosal mannitol increased the unidirectional fluxes of sodium, but not the new transport of this ion. The transport of chloride increased only in the serosal to mucosal direction yielding a net secretion of chloride equal to the change in short-circuit current. 5. The changes in potential difference and short-circuit current caused by mucosal mannitol were dependent on the presence of sodium. The changes due to serosal mannitol were dependent on both sodium and chloride. 6. Changes in undirectional transport of ions, small non-electrolytes, and water due to an osmotic gradient were attributed to changes in the dimension of the lateral intercellular spaces observed in earlier studies. 7. No evidence suggesting that the electrical changes due to the mannitol gradients could be attributed to diffusive or convective flows of fluid, but instead the changes were ascribed to perturbations in the cellular transport mechanisms.
Administration of the glucocorticoid methylprednisolone (MP) (30 mg/kg body wt for 3 days) to rats increased intestinal mucosal guanylate cyclase and Na-K-ATPase activities, short-circuit current (Isc), electrical potential difference (PD), net Na absorption, and net Cl secretion and reversed HCO3 transport from secretion to absorption. In the MP-treated animals, removal of HCO3 from both the mucosal and serosal bathing solutions increased Cl secretion but did not alter the Isc, PD, and net Na flux. Removal of Cl abolished the MP-induced increase in Isc but did not affect the MP-induced changes in net Na and HCO3 fluxes. At 6 h, after a single dose of MP, stimulation of guanylate cyclase activity was already maximal, whereas Na-K-ATPase activity was not detectably altered. The changes in intestinal transport properties present 6 h after MP treatment and associated with the increased guanylate cyclase activity were an increase in Isc and PD and a reversal of net Cl absorption to net secretion. These results suggest that an initial response to MP administration is a persistent increase in intestinal guanylate cyclase activity that mediates an electrogenic Cl secretory process, then is followed by a superimposed effect of increased Na-K-ATPase activity that mediates an increase in net Na absorption.
The mechanism of changes in small intestinal transport due to acutely increased intraluminal hydrostatic pressure (IHP) was investigated in detail using perfused in vivo rabbit intestinal segments. IHP affected passive transport in vivo by increasing effective mucosal surface area in the small intestine (indicated by 3HOH transport and tissue architectural changes) and increasing small intestinal permeability (indicated by a proportionately greater increase in mannitol than erythritol secretory clearance). IHP did not alter ileal blood flow rate measured by radioactive microspheres, despite grossly evident venous dilatation, or active intestinal transport in the ileum as measured by a) in vitro ion transport in the absence of elevated hydrostatic pressure, b) mucosal adenylate cyclase or Na-K-ATPase activities, and c) glucose-stimulated water and electrolyte absorption. Acutely increased IHP appears to influence the hydrodynamics of the mucosal microcirculation in the rabbit ileum to produce a driving force for passive filtration-secretion, which is associated with and possibly augmented by increased tissue permeability and effective surface area.
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