The Kidneys and Regulation of Water and Inorganic Ions
Chapter 14 Answers to Physiological Inquiries
Figure 14–8
GFR will decrease because the increase in plasma
osmotic force from albumin will oppose fi ltration.
Figure 14–11
Filtered load = GFR
Plasma glucose concentration
Excretion rate = Urine glucose concentration
Urine fl ow rate
Figure 14–14b
It would decrease sodium reabsorption from the
tubular fl
uid. This will result in an increase in urinary sodium
excretion. The osmotic force of sodium will carry water with
it, thus increasing urine output. Examples of such diuretics are
triamterene and amiloride.
Figure 14–17
The increased vasopressin would cause maximal
water reabsorption. Urine volume would be low (antidiuresis)
and urine osmolarity would remain high. The continuous
water reabsorption would cause a decrease in plasma sodium
concentration (hyponatremia) due to dilution of sodium.
Consequently, the plasma would have very low osmolarity. The
decreased plasma osmolarity would not inhibit vasopressin
secretion from the tumor because it is not controlled by the
hypothalamic osmoreceptors. This is called the
syndrome of
inappropriate antidiuretic hormone (SIADH)
and is one of
several possible causes of hyponatremia in humans.
Figure 14–22
Under normal conditions, the redundant control
of renin release, as indicated in this fi
gure, as well as the
participation of vasopressin (see Figure 14–24), would allow
the maintenance of normal sodium and water balance even
with denervated kidneys. However, during severe decreases
in plasma volume, like in dehydration, the denervated kidney
may not produce suffi cient renin to maximally decrease sodium
Table 14–8
The patient has respiratory acidosis with renal
compensation (hypercapnia with a normalization of arterial
pH). The patient is hypoxic, which, with normal lung function,
usually leads to hyperventilation and respiratory alkalosis.
Therefore, the patient is likely to have chronic lung disease
resulting in hypoxemia and retention of carbon dioxide
(hypercapnia). We know it is chronic because the kidneys
have had time to compensate for the acidosis by increasing
the bicarbonate added to the blood thus restoring arterial pH
almost to normal (see Figures 14–31 to 14–33).
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