Page 195 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

!
Another apparent reason is that the reabsorption-re- dosterone administration or secretion. The maxi-
lated increase in intracellular Na + concentration mum effects are observed after several hours. Al-
+
decreases the driving force for the 3 Na /Ca 2+ ex- dosterone increases Na + reabsorption, thereby
change at the basolateral cell membrane, resulting in depolarizing the luminal cell membrane (! B3).
a rise in the cytosolic Ca 2+ concentration. This rise Consequently, it increases the driving force for K +
+
acts as a signal for more frequent opening of luminal secretion and increases K conductance by increas-
+
K channels. ing the pH of the cell. Both effects lead to increased
K secretion. Aldosterone also has a very rapid (few
+
Type A intercalated cells (! B4) can active re- seconds to minutes) non-genomic effect on the cell
+
+
absorb K in addition to secreting H ions. Like membrane, the physiological significance of which +
Kidneys, Salt, and Water Balance 1. An increased K intake raises the intracellu- supply (K adaptation). Even when renal function is
the parietal cells of the stomach, their luminal
has yet to be explained.
+
The capacity of the K excretory mechanism in-
membrane contains a H /K -ATPase for this
+
+
creases in response to long-term increases in the K
purpose.
+
+
Factors that affect K excretion (! C):
impaired, this largely maintains the K balance in the
+
+
remaining, intact parts of the tubular apparatus. The
+
concentrations, which
lar and plasma K
colon can then take over more than /3 of the K ex-
+
1
thereby increases the chemical driving force
cretion.
+
for K secretion.
Mineralocortico(stero)ids. Aldosterone is the
2. Blood pH: The intracellular K conc. in renal
+
main mineralocorticoid hormone synthesized
cells rises in alkalosis and falls in acute acidosis.
This leads to a simultaneous fall in K excre-
+
adrenal cortex (! D and p. 294ff.). As with
tion, which again rises in chronic acidosis. The
other steroid hormones, aldosterone is not
stored, but is synthesized as needed. The
+
+
hibition of Na -K -ATPase reduces proximal
7 reasons for this are that (a) acidosis-related in- and secreted by the zona glomerulosa of the
Na reabsorption, resulting in increased distal principal function of aldosterone is to regulate
+
+
+
urinary flow (see no. 3), and (b) the resulting Na and K transport in the kidney, gut, and
hyperkalemia stimulates aldosterone secre- other organs (! D). Aldosterone secretion in-
tion (see no. 4). creases in response to (a) drops in blood
3. If there is increased urinary flow in the con- volume and blood pressure (mediated by an-
necting tubule and collecting duct (e.g., due to giotensin II; ! p. 184) and (b) hyperkalemia
+
a high Na intake, osmotic diuresis, or other (! D). Aldosterone synthesis is inhibited by
factors that inhibit Na + reabsorption up- atriopeptin (! p. 171 A4).
+
stream), larger quantities of K will be ex- Normal cortisol concentrations are not effective at
creted. This explains the potassium-losing ef- the aldosterone receptor only because cortisol is
fect of certain diuretics (! p. 173). The reason converted to cortisone by an 11!-hydroxysteroid ox-
for this is, presumably, that K secretion is idoreductase in aldosterone’s target cells.
+
limited at a certain luminal K concentration. Hyperaldosteronism can be either primary (al-
+
Hence, the larger the volume/time, the more dosterone-secreting tumors of adrenal cortex, as ob-
+
K taken away over time. served in Conn’s syndrome) or secondary (in volume
+
depletion, ! p. 184). Na retention resulting in high
4. Aldosterone leads to retention of Na , an in- ECF volumes and hypertension as well as a simul-
+
crease in extracellular volume (! p. 184), a taneous K losses and hypokalemic alkalosis are the
+
moderate increase in H secretion (cellular pH consequences. When more than about 90% of the
+
+
rises), and increased K excretion. It also in- adrenal cortex is destroyed, e.g. by autoimmune
creases the number of Na -K -ATPase adrenalitis, metastatic cancer or tuberculosis, pri-
+
+
molecules in the target cells and leads to a mary chronic adrenocortical insufficiency develops
chronic increase in mitochondrial density in K + (Addison’s disease). The aldosterone deficit leads to a
+
adaptation, for example (see below). sharp increase in Na excretion, resulting in hy-
+
povolemia, hypotension and K retention (hyperka-
Cellular mechanisms of aldosterone effects. The lemia). As glucocorticoid deficiency also develops,
increase in Na reabsorption is achieved by increased complications can be life-threatening, especially
+
production of transport proteins, called aldosterone- under severe stress (infections, trauma). If only one
induced proteins (AIPs). This is a genome-mediated gland is destroyed, ACTH causes hypertrophy of the
182 effect that begins approx. 30 min to 1 hour after al- other (! p. 297 A).
Despopoulos, Color Atlas of Physiology © 2003 Thieme
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