Page 193 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

+
Potassium Balance extracellular K concentration rises (especially
in non-respiratory acidosis, i.e., by 0.6 mmol/L
+
The dietary intake of K is about 100 mmol/day per 0.1 unit change in pH). Alkalosis results in
(minimum requirement: 25 mmol/day). About hypokalemia.
90% of intake is excreted in the urine, and 10% Chronic regulation of K + homeostasis is
+
+
is excreted in the feces. The plasma K conc. mainly achieved by the kidney (! B). K is sub-
normally ranges from 3.5 to 4.8 mmol/L, while ject to free glomerular filtration, and most of
+
+
intracellular K conc. can be more than 30 the filtered K is normally reabsorbed (net re-
+
+
times as high (due to the activity of Na -K - absorption). The excreted amount can, in some
Kidneys, Salt, and Water Balance comprises only about 2% of total body K , it is proximal tubule, regardless of the K supply. +
ATPase; ! A). Therefore, about 98% of the ca.
cases, exceed the filtered amount (net secre-
+
tion, see below). About 65% of the filtered K is
3000 mmol of K ions in the body are present
+
in the cells. Although the extracellular K conc.
+
reabsorbed before reaching the end of the
+
+
still very important because (a) it is needed for
This is comparable to the percentage of Na
+
and H 2O reabsorbed (! B1 and p. 157, column
regulation of K homeostasis and (b) relatively
+
+
small changes in cellular K (influx or efflux)
2). This type of K transport is mainly para-
can lead to tremendous changes in the plasma
cellular and therefore passive. Solvent drag
K conc. (with an associated risk of cardiac
lumen-positive
trans-
(! p. 24)
+
and
the
arrhythmias). Regulation of K homeostasis
epithelial potential, LPTP (! B1 and p. 162), in
+
therefore implies distribution of K through in-
+
tubule provide the driving forces for it. In the
tracellular and extracellular compartments
loop of Henle, another 15% of the filtered K is
+
+
7 and adjustment of K excretion according to K + the mid and late proximal segments of the
reabsorbed by trans- and paracellular routes
intake.
+
Acute regulation of the extracellular K + (! B2). The amount of K excreted is deter-
+
conc. is achieved by internal shifting of K be- mined in the connecting tubule and collecting
tween the extracellular fluid and intracellular duct. Larger or smaller quantities of K are then
+
fluid (! A). This relatively rapid process pre- either reabsorbed or secreted according to
vents or mitigates dangerous rises in extra- need. In extreme cases, the fractional excretion
+
+
cellular K (hyperkalemia) in cases where large of K (FE K) can rise to more than 100% in re-
quantities of K are present due to high dietary sponse to a high K intake, or drop to about
+
+
+
+
intake or internal K liberation (e.g., in sudden 3–5% when there is a K deficit (! B).
+
hemolysis). The associated K + shifting is Cellular mechanisms of renal K transport.
mainly subject to hormonal control. The insulin The connecting tubule and collecting duct con-
+
secreted after a meal stimulates Na -K - tain principal cells (! B3) that reabsorb Na +
+
+
+
ATPase and distributes the K supplied in the and secrete K . Accumulated intracellular K +
animal and vegetable cells of the food to the can exit the cell through K channels on either
+
+
cells of the body. This is also the case in diet-in- side of the cell. The electrochemical K gradient
dependent hyperkalemia, which stimulates across the membrane in question is decisive for
+
insulin secretion per se. Epinephrine likewise the efflux of K . The luminal membrane of
+
increases cellular K uptake, which is particu- principal cells also contains Na + channels
+
larly important in muscle work and trauma— through which Na enters the cell (! p. 162).
two situations that lead to a rise in plasma K . + This depolarizes the luminal membrane,
In both cases, the increased epinephrine levels which reaches a potential of about –20 mV,
+
allow the re-uptake of K in this and other cells. while the basolateral membrane maintains its
Aldosterone also increases the intracellular K + normal potential of ca. –70 mV (! B3). The
+
conc. (see below). driving force for K efflux (E m – E K, ! p. 32) is
Changes in pH affect the intra- and extra- therefore higher on the luminal side than on
+
+
cellular distribution of K (! A). This is mainly the opposite side. Hence, K preferentially exits
+
because the ubiquitous Na /H + antiporter the cell toward the lumen (secretion). This is
+
works faster in alkalosis and more slowly in mainly why K secretion is coupled with Na +
180 acidosis (! A). In acidosis, Na influx therefore reabsorption, i.e., the more Na reabsorbed by
+
+
+
+
+
decreases, Na -K -ATPase slows down, and the the principle cell, the more K secreted.
!
Despopoulos, Color Atlas of Physiology © 2003 Thieme
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