968
UNIT 4
Maintenance of the Body
25
osmotic pressure
5
25 mm Hg, capsular hydrostatic pressure
5
20 Hg.
9.
Which of the pressures that determine NFP is regulated by
both intrinsic and extrinsic controls of GFR?
For answers, see Appendix H.
Urine Formation, Step 2:
Tubular Reabsorption
Describe the mechanisms underlying water and solute
reabsorption from the renal tubules into the peritubular
capillaries.
Describe how sodium and water reabsorption are regulated
in the distal tubule and collecting duct.
Our total plasma volume filters into the renal tubules about
every 22 minutes, so all our plasma would drain away as urine
in less than 30 minutes were it not for
tubular reabsorption
,
which quickly reclaims most of the tubule contents and returns
them to the blood. Tubular reabsorption is a selective
transepi-
thelial process
that begins as soon as the filtrate enters the proxi-
mal tubules.
To reach the blood, reabsorbed substances follow either the
transcellular
or
paracellular route
(Figure 25.13)
. In the trans-
cellular route, transported substances move through the
apical
membrane
, the cytosol, and the
basolateral membrane
of the
tubule cell and then the endothelium of the peritubular cap-
illaries. Movement of substances in the paracellular route—
between
the tubule cells—is limited by the tight junctions
connecting these cells. In the proximal nephron, however,
these tight junctions are “leaky” and allow water and some im-
portant ions (Ca
2
1
, Mg
2
1
, K
1
, and some Na
1
) to pass through
the paracellular route.
Given healthy kidneys, virtually all organic nutrients such as
glucose and amino acids are completely reabsorbed to maintain
or restore normal plasma concentrations. On the other hand,
the reabsorption of water and many ions is continuously regu-
lated and adjusted in response to hormonal signals. Depending
on the substances transported, the reabsorption process may
be
active
or
passive
.
Active tubular reabsorption
requires ATP
either directly (primary active transport) or indirectly (second-
ary active transport; see Figure 3.11, p. 75) for at least one of its
steps.
Passive tubular reabsorption
encompasses diffusion, fa-
cilitated diffusion, and osmosis—processes in which substances
move down their electrochemical gradients.
±e transport mechanisms that are so important for kidney
cell function are the same ones used by all other cells. You may
wish to review these basic transport mechanisms on pp. 67–79
to refresh your memory.
Tubular Reabsorption of Sodium
Sodium ions are the single most abundant cation in the filtrate,
and about 80% of the energy used for active transport is devoted
to reabsorbing them. Sodium reabsorption is almost always ac-
tive and via the transcellular route. Let’s begin with the ATP-
driven step.
constrict, increasing peripheral resistance and bringing
blood pressure back up toward normal. ±is is the barore-
ceptor reflex we discussed in Chapter 19. As part of this
reflex, the afferent arterioles also constrict. Constriction of
the afferent arterioles decreases GFR and so helps restore
blood volume and blood pressure to normal.
2.
Renin-angiotensin-aldosterone mechanism.
As we dis-
cussed in Chapter 19 (p. 709), the
renin-angiotensin-
aldosterone mechanism
is the body’s main mechanism
for increasing blood pressure. Without adequate blood
pressure (as might be due to hemorrhage, dehydration,
etc.), glomerular filtration is not possible, so this mecha-
nism regulates GFR indirectly.
Low blood pressure causes the granular cells of the jux-
taglomerular complex to release
renin
by one or more of
three pathways:
Direct stimulation of granular cells.
As part of the
baroreceptor reflex, renal sympathetic nerves activate
β
1
-adrenergic receptors that cause the granule cells to
release renin.
Stimulation of the granular cells by input from activated
macula densa cells
. Low blood pressure or vasoconstric-
tion of the afferent arterioles by the sympathetic nervous
system reduces GFR, slowing down the flow of filtrate
through the renal tubules. When macula densa cells
sense the low NaCl concentration of this sluggishly flow-
ing filtrate, they signal the granular cells to release renin.
±ey may signal by releasing less ATP (also thought to be
the tubuloglomerular feedback messenger), by releasing
more
of the prostaglandin PGE
2
, or both.
Reduced stretch of granular cells.
Granular cells act as
mechanoreceptors. A drop in mean arterial blood pres-
sure reduces the tension in the granular cells’ plasma
membranes and stimulates them to release more renin.
Other Factors Affecting GFR
Renal cells produce a battery
of chemicals, many of which act as paracrines (local signaling
molecules) affecting renal arterioles. ±ese include
adenosine
and
prostaglandin E
2
(
PGE
2
); adenosine can be produced ex-
tracellularly from released ATP. In addition, the kidney makes
its own locally acting
angiotensin II
that reinforces the effects of
hormonal angiotensin II described in Chapter 19 (p. 707).
Homeostatic Imbalance
25.3
Abnormally low urinary output (less than 50 ml/day), called
anuria
(ah-nu
9
re-ah), may indicate that glomerular blood pres-
sure is too low to cause filtration. Renal failure and anuria can
also result from situations in which the nephrons stop function-
ing, including acute nephritis, transfusion reactions, and crush
injuries.
Check Your Understanding
7.
Extrinsic and intrinsic controls of GFR serve two different
purposes. What are they?
8.
Calculate net filtration pressure given the following values:
glomerular hydrostatic pressure
5
50 mm Hg, blood colloid
previous page 1002 Human Anatomy and Physiology (9th ed ) 2012 read online next page 1004 Human Anatomy and Physiology (9th ed ) 2012 read online Home Toggle text on/off