Chloride Absorption And Bicarbonate Secretion By The Intestinal Tract

FIGURE 4 Cellular model for Cl" absorption coupled to HCO" secretion. The mechanisms responsible for H+ and Cl" exit from the cell across the basolateral membrane are unclear.

Chloride absorption by the small and large intestines involves both paracellular and transcellular routes.

The active absorption of Na + by mechanisms a and b illustrated in Fig. 3 establishes an electrical potential difference across the intestinal epithelium oriented such that the serosal solution or plasma is electrically positive with respect to the mucosal solution or lumen. The magnitude of this electrical potential difference is determined by the rate of transcellular active Na + absorption (i.e., the ''positive current'' directed from the mucosal to the serosal solution) and the resistance of the paracellular pathways to the flow of ions. In the very leaky or low-resistance small intestine, the transepithelial electrical potential difference is small, generally between 2 and 5 mV. In the much less leaky, higher resistance large intestine, the transepithelial electrical potential difference may exceed 20 mV. These electrical potential differences provide a driving force for the absorption of Cl" by diffusion through the paracellular pathways.

Transcellular Cl" absorption involves two mechanisms by which Cl" gains entry into the absorptive cells. The first is mechanism (c) illustrated in Fig. 3, in which Cl" entry is coupled to the entry (cotransport) of Na + and, often, K + ; this mechanism can be blocked by so-called ''loop diuretics'' such as furosemide. The second is a countertransport mechanism that brings about Cl" entry across the apical membrane in exchange for HCO", which is produced within the cell by the hydration of CO2 catalyzed by carbonic anhydrase (Fig. 4). Both entry mechanisms are present in small intestinal absorptive cells, but only the HCO" exchange mechanism is found in the colon, where it is responsible for the alkaline pH of fecal water. Both processes are capable of driving Cl" into the cell against an electrochemical potential difference; that is, they are examples of secondary active transport. In the first instance, the energy for the uphill movement of Cl" is derived from coupling to the downhill movement of Na + into the cell; in the second instance, it is derived from coupling to the downhill movement of HCO" out of the cell.

The mechanisms responsible for Cl" exit from the cells across the basolateral membranes are unclear. But, inasmuch as intracellular Cl" is at a higher electrochemical potential than that in the serosal fluid or plasma, some of the Cl" may exit the cell by diffusion.

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