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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