Potassium Transport By The Intestines

K+ is both absorbed and secreted by the intestines. The bulk of the K + that enters the intestinal tract, derived from salivary, gastric, pancreatic, and biliary secretions as well as dietary intake, is reabsorbed in the small intestine. The primary mechanism responsible is probably diffusion through paracellular pathways. Thus, the reabsorption of water, secondary to the active absorption of Na + and other solutes (see below), will tend to concentrate K + in the chyme. But, as noted earlier, because the junctional complexes in the small intestine are very leaky to small ions, large concentration differences between the chyme and plasma cannot be sustained. Thus, the reabsorption of water establishes a concentration difference for 5+ between chyme and plasma that serves as the driving force for K+ diffusion through paracellular pathways from the former to the latter. In contrast to the situation in the small intestine, K+ is also absorbed by the colon by means of a K + ,H + -ATPase located in the apical membrane of the surface epithelial cell. K+ that is pumped into the cell in exchange for H+ then exits across K+ channels

FIGURE 5 Cellular model for K+ secretion by colonic epithelial cells.

located in the basolateral membrane. The activity of the K + ,H + -ATPase appears to be upregulated by K + depletion and acidosis.

K+ is also actively secreted by colonic epithelial cells by the mechanism illustrated in Fig. 5. The apical membranes of these cells appear to be permeable to K + . Thus, some of the K+ pumped into the cell by the Na + -K + pump at the basolateral membranes does not recycle across those barriers but, instead, exits across the apical membranes. This is responsible for the high K + concentration in fecal water. But, inasmuch as the total fecal water is normally only 100-200 mL/day, the actual amount of K+ normally lost in the excreta is small. Finally, as noted earlier, aldosterone stimulates Na+ absorption by colonic cells and, by virtue of the mechanism illustrated in Fig. 5, also increases K + secretion by these cells. Thus, the effects of aldosterone in the colon closely resemble those in the distal nephron (see Chapter 32).

These observations gave rise to the notions that water absorption is secondary to solute absorption and is a passive process driven solely by osmotic forces, and that the osmolarity of the absorbate is determined by the hydraulic permeability or filtration coefficient (see Chapter 2) of the transcellular and paracellular pathways. The models that have emerged to explain the observations illustrated in Fig. 6 are shown in Fig. 7.

Figure 7A is a model of a leaky epithelium, such as the small intestine, where the apical and basolateral membranes are permeable to water and the junctional complexes are highly permeable to both water and small ions, such as Na + , K + , and Cl". In this model, the apical and basolateral membrane mechanisms responsible for the transcellular absorption of Na + , Cl", sugars, amino acids, and other solutes deposit the solutes in the confined regions that surround the basolateral membrane: the intercellular spaces and the subepithelial spaces. This increases the osmolarity of those regions and establishes the driving force for water absorption. Inasmuch as the pathways for water flow are highly permeable to water, very small differences in osmolarity amounting to only a few mOsm/L are sufficient to keep the flow of water close to the flow of solutes in nearly isotonic proportions. Thus, as in the renal proximal tubule (see Chapter 29), fluid absorption by the very leaky small intestine is essentially isosmotic; in other works the osmolarity of the luminal contents does not differ from that of the plasma by more than a few mOsm/L. Further, as mentioned earlier, because of the leakiness of the junctions, the concentrations of Na + , Cl", and K+ in the luminal fluid do not differ markedly from those in the plasma. Finally, because the junctions are leaky to these small ions, the flow of water through these junctions entraps and drags these small ions along; this phenomenon is referred to as solvent drag, and it serves to augment ion absorption by the small intestine.

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