CELLULAR MECHANISMS OF K+ ABSORPTION AND SECRETION (GI Tract)

The pattern of intestinal K⁺ movement parallels that of the kidney: (1) the intestines have the capacity for both K⁺ absorption and secretion, and (2) the intestines absorb K⁺ in the proximal segments but secrete it in the distal segments

Dietary K⁺ furnishes 80 to 120 mmol/day, whereas stool K⁺ output is only ~10 mmol/day. The kidney is responsible for disposal of the remainder of the daily K⁺ intake

Substantial quantities of K⁺ are secreted in gastric, pancreatic, and biliary fluid. Therefore, the total K⁺ load presented to the small intestine is considerably greater than that represented by the diet

K⁺ Absorption in the small intestine

Studies in which a plasma-like solution is perfused through segments of the intestine established that K⁺ is absorbed in the jejunum and ileum of the small intestine and is secreted in the large intestine. Although the small intestine absorbs substantial amounts of K⁺, no evidence has been presented to suggest that K⁺ absorption in the jejunum and ileum is an active transport process or even carrier mediated. Thus, K⁺ absorption in the small intestine is probably passive, most likely a result of solvent drag

Although changes in dietary Na⁺ and K⁺ and alterations in hydration influence K⁺ movement in the colon, similar physiological events do not appear to affect K⁺ absorption in the small intestine

Colonic secretion

This secretion occurs by two mechanisms: a passive transport process and an active process

Passive K⁺ secretion: is driven by the lumen-negative V_TE of 15 to 25 mV. The route of passive K⁺ secretion is predominantly para-cellular, not transcellular. Because V_TE is the primary determinant of passive K⁺ secretion, it is not surprising that passive K⁺ secretion is greatest in the distal end of the colon, where V_TE difference is most negative.

Similarly, increases in the lumen-negative V_TE that occur as an adaptive response to dehydration or secondary to an elevation in aldosterone secretion—result in an enhanced rate of passive K⁺ secretion

Colonic Active K⁺ secretion

Active transport of K⁺ is subject to considerable segmental variation in the colon. Whereas active K⁺ secretion occurs throughout the colon, active K⁺ absorption is present only in the distal segments of the large intestine. Thus, in the rectosigmoid colon, active K⁺ absorption and active K⁺ secretion are both operative and appear to contribute to total body homeostasis.

The general paradigm of active K⁺ transport in the colon is a pump-leak model. Uptake of K⁺ across the basolateral membrane is a result of both the Na-K pump and the Na/K/Cl cotransporter (NKCC1), which is energized by the low [Na⁺]_i that is created by the Na-K pump. Once K⁺ enters the cell across the basolateral membrane, it may exit either across the apical membrane (K⁺ secretion) or across the basolateral membrane (K⁺ recycling)

When apical K⁺ channel activity is less than basolateral channel activity, K⁺ recycling dominates. Indeed, in the basal state, the rate of active K⁺ secretion is low

It is likely that aldosterone stimulates active K⁺ secretion in surface epithelial cells of the large intestine, whereas cAMP enhances active K⁺ secretion in crypt cells. In both cases, the rate-limiting step is the apical BK K⁺ channel, and both secretagogues act by increasing K⁺ channel activity

Colonic Active K⁺ absorption

The mechanism of active K⁺ absorption appears to be an exchange of luminal K⁺ for intracellular H⁺ across the apical membrane, mediated by an H-K pump

Colonic K⁺ movement through the active K⁺ absorption process occurs through a transcellular route, in contrast to the para-cellular route that characterizes K⁺ absorption in the small intestine

The mechanism of K⁺ exit across the basolateral membrane may involve K/Cl cotransport. Not known is whether active K⁺ secretion and active K⁺ absorption occur in the same cell or in different cells