Answers to Test & Quantitative and Thought Questions
The main driving force favoring ﬂ uid ﬁ ltration
from the glomerular capillary to Bowman’s space is
glomerular capillary blood pressure (
In order for a substance to appear in the urine at
a faster rate than its ﬁ ltration rate, it must also be
actively secreted into the tubular ﬂ
Excessive sweating will decrease blood volume. This
will lead to compensatory mechanisms to preserve
total body water, including a decrease in urine
Urea is trapped in the medullary interstitium and
is an osmotically active particle. The resultant
increase in tonicity helps to maintain the gradient for
medullary passive water reabsorption.
A decrease in sodium intake stimulates renin because
of the decrease in sodium delivery to the macula
densa. This is detected and results in an increase in
renin release from the juxtaglomerular cells.
Parathyroid hormone stimulates calcium
reabsorption in the distal tubules of the nephron,
thereby decreasing calcium excretion. Because
parathyroid hormone is increased in hypocalcemic
states, the resulting decrease in calcium excretion
helps to restore blood calcium to normal.
Secretion of ammonium into the renal tubule is
one way to rid the body of excess hydrogen ion
Increases in ventilation greater than metabolic rate
“blow off” CO
and results in a decrease in arterial
. Because of the buffering of bicarbonate, this
increases arterial pH (respiratory alkalosis).
Cortical nephrons either have short or absent
Henle’s loops. Only juxtamedullary nephrons have
long Henle’s loops, which plunge into the renal
medulla and create a hyperosmotic interstitium via
When the renal corpuscles become diseased, they
greatly increase their permeability to protein.
Furthermore, diseased proximal tubules cannot
remove the ﬁ ltered protein from the tubular lumen.
This results in increased protein in the urine
Quantitative and Thought Questions
No. These are possibilities, but there is another.
Substance T may be secreted by the tubules.
No. It is a possibility, but there is another. Substance
V may be ﬁ ltered and/or secreted, but the substance
V entering the lumen via these routes may be
125 mg/min. The amount of any substance ﬁ ltered
per unit time is given by the product of the GFR
and the ﬁ lterable plasma concentration of the
substance—in this case, 125 ml/min × 100 mg/
100 ml = 125 mg/min.
The plasma concentration might be so high that the
for the amino acid is exceeded, so all the ﬁ ltered
amino acid is not reabsorbed. A second possibility is
that there is a speciﬁ c defect in the tubular transport
for this amino acid. A third possibility is that some
other amino acid is present in the plasma in high
concentration and is competing for reabsorption.
No. Urea is ﬁ ltered and then partially reabsorbed. The
reason its concentration in the tubule is higher than in
the plasma is that relatively more water is reabsorbed
than urea. Therefore, the urea in the tubule becomes
concentrated. Despite the fact that urea
in the urine is greater than in the plasma, the
is less than the ﬁ ltered load (that is, net
reabsorption has occurred).
They would all be decreased. The transport of all
these substances is coupled, in one way or another, to
that of sodium.
GFR would not go down as much, and renin secretion
would not go up as much as in a person not receiving
the drug. The sympathetic nerves are a major pathway
for both responses during hemorrhage.
There would be little if any increase in aldosterone
secretion. The major stimulus for increased
aldosterone secretion is angiotensin II, but this
substance is formed from angiotensin I by the action
of angiotensin-converting enzyme, and so blockade of
this enzyme would block the pathway.
(b) Urinary excretion in the steady state must be less
than ingested sodium chloride by an amount equal to
that lost in the sweat and feces. This is normally quite
small, less than 1 g/day, so that urine excretion in this
case equals approximately 11 g/day.
If the hypothalamus had been damaged, there might be
inadequate secretion of ADH. This would cause loss of
a large volume of urine, which would tend to dehydrate
the person and make her thirsty. Of course, the area of
the brain involved in thirst might have suffered damage.
This is primary aldosteronism or Conn’s syndrome.
Because aldosterone stimulates sodium reabsorption
and potassium secretion, there will be total-body
retention of sodium and loss of potassium. Interestingly,
the person in this situation actually retains very little
sodium because urinary sodium excretion returns to
normal after a few days despite the continued presence
of the high aldosterone. One explanation for this is
that GFR and atrial natriuretic factor both increase as a
result of the initial sodium retention.
Sodium and water balance would become negative
because of increased excretion of these substances in
the urine. The person would also develop a decreased
plasma bicarbonate concentration and metabolic
acidosis because of increased bicarbonate excretion.
The effects on acid-base status are explained by the
fact that hydrogen ion secretion—blocked by the
drug—is needed both for bicarbonate reabsorption
and for the excretion of hydrogen ion (contribution of
new bicarbonate to the blood). The increased