972
UNIT 4
Maintenance of the Body
25
Atrial natriuretic peptide (ANP).
In contrast to aldoste-
rone, which acts to conserve Na
1
, ANP reduces blood Na
1
,
thereby decreasing blood volume and blood pressure. Re-
leased by cardiac atrial cells when blood volume or blood
pressure is elevated, ANP exerts several effects that lower
blood Na
1
content, including direct inhibition of Na
1
reab-
sorption at the collecting ducts.
Parathyroid hormone (PTH).
Acting primarily at the DCT,
PTH increases the reabsorption of Ca
2
1
.
Urine Formation, Step 3: Tubular Secretion
Describe the importance of tubular secretion and list
several substances that are secreted.
±e most important way to clear plasma of unwanted sub-
stances is to simply not reabsorb them from the filtrate. Another
way is
tubular secretion
—essentially, reabsorption in reverse.
Tubular secretion moves
selected
substances (such as H
1
, K
1
,
NH
4
1
, creatinine, and certain organic acids and bases) from the
peritubular capillaries through the tubule cells into the filtrate.
Also, some substances (such as HCO
3
2
) that are synthesized in
the tubule cells are secreted.
±e urine eventually excreted contains
both filtered and se-
creted substances
. With one major exception (K
1
), the PCT is
the main site of secretion, but the cortical parts of the collecting
ducts are also active
(Figure 25.15)
.
Tubular secretion is important for
Disposing of substances, such as certain drugs and metabolites,
that are tightly bound to plasma proteins.
Because plasma
proteins are generally not filtered, the substances they bind
are not filtered and so must be secreted.
Eliminating undesirable substances or end products that have
been reabsorbed by passive processes.
Urea and uric acid, two
nitrogenous wastes, are both handled in this way. Urea han-
dling in the nephron is complicated and will be discussed
on p. 976, but the net effect is that 40–50% of the urea in the
filtrate is excreted.
Ridding the body of excess K
1
. Because virtually all K
1
present
in the filtrate is reabsorbed in the PCT and ascending nephron
loop, nearly all K
1
in urine comes from aldosterone-driven
active tubular secretion into the late DCT and collecting
ducts.
Controlling blood pH.
When blood pH drops toward the
acidic end of its homeostatic range, the renal tubule cells ac-
tively secrete more H
1
into the filtrate and retain and gener-
ate more HCO
3
2
(a base). As a result, blood pH rises and the
urine drains off the excess H
1
. Conversely, when blood pH
approaches the alkaline end of its range, Cl
2
is reabsorbed
instead of HCO
3
2
, which is allowed to leave the body in
urine. We will discuss the kidneys’ role in pH homeostasis in
more detail in Chapter 26.
Figure 25.15 summarizes tubular reabsorption and secretion
in the various parts of the nephron and collecting duct.
±e rule for water is that it leaves the descending (but not the
ascending) limb of the nephron loop. ±e opposite is true for
solutes. Virtually no solute reabsorption occurs in the descend-
ing limb, but solutes are reabsorbed both actively and passively
in the ascending limb.
In the thin segment of the ascending limb, Na
1
moves
passively down the concentration gradient created by water
reabsorption. In the thick ascending limb, a Na
1
-K
1
-2Cl
2
sym-
porter is the main means of Na
1
entry at the apical surface. A
Na
1
-K
1
ATPase operates at the basolateral membrane to create
the ionic gradient that drives the symporter. ±e thick ascend-
ing limb also has Na
1
-H
1
antiporters. In addition, some 50% of
Na
1
passes via the paracellular route in this region.
Distal Convoluted Tubule and Collecting Duct
While reab-
sorption in the PCT and nephron loop does not vary with the
body’s needs, reabsorption in the DCT and collecting duct
is fine-tuned by hormones. Because most of the filtered wa-
ter and solutes have been reabsorbed by the time the DCT is
reached, only a small amount of the filtered load is subject to
this fine tuning (e.g., about 10% of the originally filtered NaCl
and 25% of the water). We introduce hormones that act at the
DCT and collecting duct here but discuss them in more detail
in Chapter 26.
Antidiuretic hormone (ADH).
As its name reveals, ADH
inhibits
diuresis
(di
0
u-re
9
sis), or urine output. ADH makes
the principal cells of the collecting ducts more permeable to
water by causing aquaporins to be inserted into their apical
membranes. ±e amount of ADH determines the number of
aquaporins, and thus the amount of water that is reabsorbed
there. When the body is overhydrated, extracellular fluid os-
molality decreases, decreasing ADH secretion by the poste-
rior pituitary (see p. 599) and making the collecting ducts
relatively impermeable to water. ADH also increases urea
reabsorption by the collecting ducts, as we will describe later.
Aldosterone.
Aldosterone fine-tunes reabsorption of the re-
maining Na
1
. Decreased blood volume or blood pressure, or
high extracellular K
1
concentration (hyperkalemia), can cause
the adrenal cortex to release aldosterone to the blood. Except
for hyperkalemia (which
directly
stimulates the adrenal cortex
to secrete aldosterone), these conditions promote the renin-
angiotensin-aldosterone mechanism (see Figure 25.12).
Aldosterone targets the principal cells of the collecting
ducts and cells of the distal portion of the DCT (prodding
them to synthesize and retain more apical Na
1
and K
1
chan-
nels, and more basolateral Na
1
-K
1
ATPases). As a result, little
or no Na
1
leaves the body in urine. In the absence of aldo-
sterone, these segments reabsorb much less Na
1
and about
2% of Na
1
filtered daily can be lost—an amount incompatible
with life.
Physiologically, aldosterone’s role is to increase blood
volume, and therefore blood pressure, by enhancing Na
1
reabsorption. In general, water follows Na
1
if aquaporins are
present. Aldosterone also reduces blood K
1
concentrations
because aldosterone-induced reabsorption of Na
1
is coupled
to K
1
secretion in the principal cells of the collecting duct.
±at is, as Na
1
enters the cell, K
1
moves into the lumen.
previous page 1006 Human Anatomy and Physiology (9th ed ) 2012 read online next page 1008 Human Anatomy and Physiology (9th ed ) 2012 read online Home Toggle text on/off