Tuesday, July 21, 2015

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 VTE of 15 to 25 mV. The route of passive K+ secretion is predominantly para-cellular, not transcellular. Because VTE 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 VTE difference is most negative.
Similarly, increases in the lumen-negative VTE 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

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