510
Chapter 14
termed
pressure natriuresis
(“natriuresis” means increased
urinary sodium loss). The actual transduction mechanism of
this direct effect is unknown.
Thus, an increased blood pressure reduces sodium
reabsorption by two mechanisms: It reduces the activity of
the renin-angiotensin-aldosterone system, and it also acts
locally on the tubules. Conversely, a decreased blood pressure
decreases sodium excretion both by stimulating the renin-
angiotensin-aldosterone system and by acting on the tubules
to enhance sodium reabsorption.
Now is a good time to look back at Figure 12–57, which
describes the strong causal, reciprocal relationship between arte-
rial blood pressure and blood volume, the result of which is that
blood volume is perhaps the major long-term determinant of
blood pressure. The direct effect of blood pressure on sodium
excretion is, as Figure 12–57 shows, one of the major links
in these relationships. An important hypothesis is that most
people who develop hypertension do so because their kidneys,
for some reason, do not excrete enough sodium in response to
a normal arterial pressure. Consequently, at this normal pres-
sure, some dietary sodium is retained, which causes the pres-
sure to rise enough to produce adequate sodium excretion to
balance sodium intake, although at an increased body sodium
content.
Renal Water Regulation
Water excretion is the difference between the volume of water fi l-
tered (the GFR) and the volume reabsorbed. Thus, the changes
in GFR initiated by baroreceptor afferent input described in the
previous section tend to have the same effects on water excre-
tion as on sodium excretion. As is true for sodium, however,
the rate of water reabsorption from the tubules is the most
important factor determining how much water is excreted. As
we have seen, this is determined by vasopressin, and so total-
body water is regulated mainly by refl
exes that alter the secre-
tion of this hormone.
As described in Chapter 11, vasopressin is produced by
a discrete group of hypothalamic neurons whose axons termi-
nate in the posterior pituitary, which releases vasopressin into
the blood. The most important of the inputs to these neurons
come from baroreceptors and osmoreceptors.
Baroreceptor Control of Vasopressin Secretion
A decreased extracellular fl uid volume, due for example, to diar-
rhea or hemorrhage, elicits an increase in aldosterone release
via activation of the renin-angiotensin system. However, the
decreased extracellular volume also triggers an increase in
vasopressin secretion. This increased vasopressin increases the
water permeability of the collecting ducts. More water is pas-
sively reabsorbed and less is excreted, so water is retained to
help stabilize the extracellular volume.
This refl ex is initiated by several baroreceptors in the car-
diovascular system (
Figure 14–24
). The baroreceptors decrease
their rate of fi ring when cardiovascular pressures decrease, as
H
2
O excretion
Plasma vasopressin
Posterior pituitary
Vasopressin secretion
Venous, atrial, and arterial
pressures
Collecting ducts
Tubular permeability
to H
2
O
H
2
O reabsorption
Plasma volume
Reflexes mediated
by cardiovascular
baroreceptors
(see Fig. 14–20)
Figure 14–24
Baroreceptor pathway by which vasopressin secretion increases
when plasma volume decreases. The opposite events (culminating
in a decrease in vasopressin secretion) occur when plasma volume
increases.
Kidneys
Tubules
Na
+
reabsorption
Arterioles
Afferent dilation;
efferent constriction
GFR
Plasma ANP
Plasma volume
Cardiac atria
Distension
ANP secretion
Sodium excretion
Plasma
aldosterone
Figure 14–23
Atrial natriuretic peptide (ANP) increases sodium excretion.
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