Page 1035 - Fundamentals of anatomy physiology

1022 Unit 5 Environmental Exchange
2. It establishes a concentration gradient that permits the pas- Secretion at the DCT
sive reabsorption of water from the tubular fluid in the col-
lecting system. Circulating levels of antidiuretic hormone
(ADH) regulate this reabsorption.
In summary, countercurrent multiplication is a way to
either concentrate or dilute urine. The tubular fluid entering
the descending limb of the nephron loop has an osmotic
concentration of roughly 300 mOsm/L, due primarily to the
presence of ions such as Na+ and CI−. The concentration of
organic wastes, such as urea, is low. About half of the tubular
fluid entering the nephron loop is then reabsorbed along
the thin descending limb. Two-thirds of the Na+ and CI− is
reabsorbed along the thick ascending limb. As a result, the
DCT receives a reduced volume of tubular fluid with an os-
motic concentration of about 100 mOsm/L. Urea and other
organic wastes, which were not pumped out of the thick as-
cending limb, now represent a significant proportion of the
dissolved solutes.
Reabsorption and Secretion at the DCT
As we have just seen, the composition and volume of tubular
fluid change dramatically as it flows from the capsular space
to the distal convoluted tubule. Only 15–20 percent of the
initial filtrate volume reaches the DCT. The concentrations of
electrolytes and organic wastes in the arriving tubular fluid no
longer resemble the concentrations in blood plasma. Selective
reabsorption or secretion, primarily along the DCT, makes the
final adjustments in the solute composition and volume of the
tubular fluid.
26 Reabsorption at the DCT
Throughout most of the DCT, the tubular cells actively trans-
port Na+ and CI− out of the tubular fluid (Figure 26–14a).
Tubular cells along the distal portions of the DCT also con-
tain ion pumps that reabsorb tubular Na+ in exchange for
another cation (usually K+) (Figure 26–14b). The hormone
aldosterone, produced by the adrenal cortex, controls the Na+
channels and the ion pump. This hormone stimulates the
synthesis and incorporation of sodium channels and sodium
ion pumps in plasma membranes along the DCT and col-
lecting duct. The net result is a reduction in the number of
sodium ions lost in urine.
However, sodium ion conservation is associated with po-
tassium ion loss. Prolonged aldosterone stimulation can there-
fore produce hypokalemia, a dangerous reduction in the plasma
K+ concentration. The secretion of aldosterone and its actions
on the DCT and collecting system are opposed by the natri-
uretic peptides (ANP and BNP).
The DCT is also the primary site of Ca2+ reabsorption. Cir-
culating levels of parathyroid hormone and calcitriol regulate
this process. pp. 656–657
The blood entering the peritubular capillaries still contains
a number of potentially undesirable substances that did not
cross the filtration membrane at the glomerulus. In most cases,
the concentrations of these substances are too low to cause
physiological problems. However, any ions or compounds in
peritubular capillaries will diffuse into the peritubular fluid. If
those concentrations become too high, the tubular cells may
absorb these substances from the peritubular fluid and secrete
them into the tubular fluid. Table 26–3 (p. 1012) lists some of
the substances secreted into tubular fluid by the proximal and
distal convoluted tubules.
The rate of K+ and H+ secretion increases or decreases
in response to changes in their concentrations in peritubular
fluid. The higher their concentration in the peritubular fluid,
the higher the rate of secretion. Potassium and hydrogen ions
merit special attention, because their concentrations in body
fluids must be maintained within narrow limits.
Potassium Ion Secretion. Figure 26–14a,b diagrams the
mechanism of K+ secretion. In effect, tubular cells trade so-
dium ions in the tubular fluid for excess potassium ions in
body fluids. Potassium ions are removed from the peritubu-
lar fluid in exchange for sodium ions from the tubular fluid.
These potassium ions diffuse into the lumen of the DCT
through potassium leak channels at the apical surfaces of the
tubular cells.
Hydrogen Ion Secretion. Hydrogen ion secretion is also
associated with the reabsorption of sodium. Figure 26–14c
depicts two routes of secretion. Both involve the genera-
tion of carbonic acid by the enzyme carbonic anhydrase.
pp. 888, 926 Hydrogen ions generated by the dissociation
of the carbonic acid are secreted by sodium-linked coun-
tertransport in exchange for Na+ in the tubular fluid. The
bicarbonate ions diffuse into the peritubular fluid and then
into the bloodstream. There they help prevent changes in
plasma pH.
Hydrogen ion secretion acidifies the tubular fluid while
increasing the pH of the blood. Hydrogen ion secretion speeds
up when the pH of the blood decreases. This can happen in
lactic acidosis, which can develop after exhaustive muscle activ-
ity, or ketoacidosis, which can develop in starvation or diabe-
tes mellitus. p. 982 The combination of H+ removal and
HCO3− production by the kidneys plays an important role in
the control of blood pH. Because one of the secretory pathways
is aldosterone sensitive, aldosterone stimulates H+ secretion.
Prolonged aldosterone stimulation can cause alkalosis, or ab-
normally high blood pH.
In Chapter 25, we noted that the production of lactic
acid and ketone bodies during the postabsorptive state could
cause acidosis. Under these conditions, the PCT and DCT