790
UNIT FIVE
atria of the heart stretch due to increased blood volume. ANP
stimulates sodium excretion through a number of mecha-
nisms, including increasing GFR.
Eating raw spinach or undercooked hamburger, drinking unpro-
cessed apple cider, and petting animals at country fairs have all led to
hemolytic uremic syndrome (HUS). The direct cause is a poison called
shigatoxin that a certain strain of
E. coli
(bacteria) produces. The toxin
finds its way to humans through excrement—in the water used
to grow spinach, in beef mixed from many exposed animals, from
apples that dropped into droppings, and from tiny hands petting ani-
mals. Food poisoning from toxin-producing
E. coli
begins with sharp
abdominal pain and bloody diarrhea, and about 16% of the time HUS
develops. About 5% of HUS cases are fatal.
Shigatoxin causes ±
brin to form thrombi that obstruct the nar-
row glomerular capillaries. Platelets join the clumping, depleting the
circulation of these cell fragments (thrombocytopenia). Red blood
cells in the blocked glomerular capillaries break apart, causing hemo-
lytic anemia. As GFR plummets, the person, typically a child, goes into
acute renal failure.
Tubular Reabsorption
If the composition of the glomerular ±
ltrate entering the renal
tubule is compared with that of the urine leaving the tubule,
it is apparent that the fl
uid changes as it passes through the
tubule (see table 20.1). For example, glucose is present in
the ±
ltrate but absent in the urine. In contrast, urea and uric
acid are considerably more concentrated in urine than they
The volume of plasma the kidneys ± lter also depends on
the
surface area
of the glomerular capillaries. This surface
area is estimated to be about 2 square meters—approximately
equal to the surface area of an adult’s skin.
PRACTICE
10
What processes occur as urine forms?
11
How is ±
ltration pressure calculated?
12
What factors in²
uence the rate of glomerular ±
ltration?
Control of Filtration Rate
In general, glomerular ±
ltration rate remains relatively con-
stant through a process called
autoregulation.
However, cer-
tain conditions override autoregulation. GFR may increase,
for example, when body fl
uids are in excess and decrease
when the body must conserve fl
uid.
Recall from chapter 15 (p. 587) that sympathetic nervous
system ± bers synapse with the vascular smooth muscle of
arterioles. Refl
exes responding to changes in blood pressure
and volume control the activity of these sympathetic ±
bers.
If blood pressure and volume drop, vasoconstriction of the
afferent arterioles results, decreasing ±
ltration pressure and
thus GFR. The result is an appropriate decrease in the rate
of urine formation when the body must conserve water. If
receptors detect excess body fl
uids, vasodilation of the affer-
ent arteriole results, increasing ±
ltration pressure and GFR.
A second control of GFR is the hormonelike
renin-
angiotensin system.
The juxtaglomerular cells of the affer-
ent arterioles secrete an enzyme,
renin,
in response to
stimulation from sympathetic nerves and pressure-sensitive
cells, called
renal baroreceptors,
in the afferent arteriole.
These factors stimulate renin secretion if blood pressure
drops. The macula densa also controls renin secretion. Cells
of the macula densa sense the concentrations of sodium,
potassium, and chloride ions in the distal renal tubule.
Decreasing levels of these ions stimulate renin secretion.
Once in the bloodstream,
renin
reacts with the plasma
protein
angiotensinogen
to form
angiotensin I.
An enzyme,
angiotensin-converting enzyme
(ACE), on capillary endothe-
lial cells (particularly in the lungs), rapidly converts angio-
tensin I to
angiotensin II
(f g. 20.20)
.
Angiotensin II has a number of renal effects that help
maintain sodium balance, water balance, and blood pressure.
As a vasoconstrictor, angiotensin II affects both the afferent
and efferent arterioles. Although afferent arteriolar constric-
tion decreases GFR, efferent arteriolar constriction minimizes
the decrease, thus contributing to autoregulation of GFR.
Angiotensin II has a major effect on the kidneys through
the adrenal cortical hormone aldosterone, which stimulates
sodium reabsorption in the distal convoluted tubule. By stim-
ulating aldosterone secretion, angiotensin II helps to reduce
the amount of sodium excreted in the urine. Angiotensin II
also stimulates ADH secretion, helping to retain water.
The hormone
atrial natriuretic peptide
(ANP) also
affects sodium excretion. ANP secretion increases when the
FIGURE 20.20
The formation of angiotensin II in the bloodstream
involves several organs and results in multiple actions that conserve
sodium and water.
Bloodstream
Angiotensin I
Liver
Kidney
Lung capillaries
Angiotensin II
• Vasoconstriction
• Increased
aldosterone
secretion
• Increased
ADH secretion
• Increased thirst
Angiotensinogen
Renin
Angiotensin-
converting
enzyme
Release into
bloodstream
Stimulation
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