The Kidneys and Regulation of Water and Inorganic Ions
lar volume comprises plasma volume and interstitial volume,
plasma volume is also directly related to total-body sodium. We
saw in Chapter 12 that plasma volume is an important determi-
nant of the blood pressures in the veins, cardiac chambers, and
arteries. Thus, the chain linking total-body sodium to cardio-
vascular pressures is completed: low total-body sodium leads
to low plasma volume, which leads to low cardiovascular pres-
sures. These low pressures, via baroreceptors, initiate refl exes
that infl uence the renal arterioles and tubules so as to lower
GFR and increase sodium reabsorption. These latter events
decrease sodium excretion, thereby retaining sodium in the
body and preventing further decreases in plasma volume and
cardiovascular pressures. Increases in total-body sodium have
the reverse refl ex effects.
To summarize, the amount of sodium in the body deter-
mines the extracellular fl uid volume, the plasma volume com-
ponent of which helps determine cardiovascular pressures,
which initiate the responses that control sodium excretion.
Control of GFR
Figure 14–20
summarizes the major mechanisms by which an
example of increased sodium loss elicits a decrease in GFR. The
main direct cause of the reduced GFR is a reduced net glomeru-
lar fi ltration pressure. This occurs both as a consequence of a
lowered arterial pressure in the kidneys and, more importantly,
as a result of refl exes acting on the renal arterioles. Note that
these refl exes are the basic baroreceptor refl exes described in
Chapter 12—a decrease in cardiovascular pressures causes neu-
rally mediated refl ex vasoconstriction in many areas of the body.
As we will see later, the hormones angiotensin II and vasopres-
sin also participate in this renal vasoconstrictor response.
Conversely, an increase in GFR is usually elicited by
neuroendocrine inputs when an increased total-body sodium
level increases plasma volume. This increased GFR contributes
to the increased renal sodium loss that returns extracellular
volume to normal.
Control of Sodium Reabsorption
For the long-term regulation of sodium excretion, the control
of sodium reabsorption is more important than the control of
GFR. The major factor determining the rate of tubular sodium
reabsorption is the hormone aldosterone.
Aldosterone and the Renin-Angiotensin System
The adrenal cortex produces a steroid hormone,
which stimulates sodium reabsorption by the distal convoluted
tubule and the cortical collecting ducts. An action affecting
these late portions of the tubule is just what one would expect
for a fi ne-tuning input because most of the fi ltered sodium
has been reabsorbed by the time the fi ltrate reaches the distal
parts of the nephron. When aldosterone is completely absent,
approximately 2 percent of the fi ltered sodium (equivalent
to 35 g of sodium chloride per day) is not reabsorbed, but
excreted. In contrast, when the plasma concentration of aldo-
sterone is high, essentially all the sodium reaching the distal
tubule and cortical collecting ducts is reabsorbed. Normally,
the plasma concentration of aldosterone and the amount of
sodium excreted lie somewhere between these extremes.
As opposed to vasopressin, which is a peptide and acts
quickly, aldosterone is a steroid and acts more slowly because
it induces changes in gene expression and protein synthesis.
In the case of the nephron, the proteins participate in sodium
transport. Look again at Figure 14–14b. Aldosterone induces
Constriction of afferent renal arterioles
Net glomerular filtration pressure
and H
O excreted
Activity of renal
sympathetic nerves
Arterial blood pressure
Cardiac output
Ventricular end–diastolic
Atrial pressure
Venous return
Venous pressure
Plasma volume
and H
O loss
due to diarrhea
Stroke volume
mediated by
venous, atrial,
and arterial
Figure 14–20
Direct and neurally mediated refl ex pathways by which the GFR
and thus sodium and water excretion decrease when plasma volume
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