Human Physiology, 14th edition (2016)

Physiology of the Kidneys 589

Figure 17.10 The formation of glomerular
ultrafiltrate. Only a very small proportion of plasma proteins
( green spheres ) are filtered, but smaller plasma solutes ( purple
spheres ) easily enter the glomerular ultrafiltrate. Arrows indicate
the direction of filtration.

Glomerular

(Bowman’s)

capsule

Glomerular

ultrafiltrate

Efferent

arteriole

Protein

Other

solutes

Afferent

arteriole

arterioles result from both extrinsic regulatory mechanisms
(produced by sympathetic nerve innervation) and intrinsic
regulatory mechanisms (those within the kidneys, also termed
renal autoregulation ). These mechanisms are needed to ensure
that the GFR will be high enough to allow the kidneys to elimi-
nate wastes and regulate blood pressure, but not so high as to
cause excessive water loss.

Sympathetic Nerve Effects

An increase in sympathetic nerve activity, as occurs during the
fight-or-flight reaction and exercise, stimulates constriction
of afferent arterioles. This helps preserve blood volume and
divert blood to the muscles and heart. A similar effect occurs
during cardiovascular shock, when sympathetic nerve activ-
ity stimulates vasoconstriction. The decreased GFR and the
resulting decreased rate of urine formation help compensate
for the rapid drop in blood pressure under these circumstances
( fig. 17.11 ).

Renal Autoregulation

When the direct effect of sympathetic stimulation is experi-
mentally removed, the effect of systemic blood pressure on
GFR can be observed. Under these conditions, surprisingly, the
GFR remains relatively constant despite changes in mean arte-
rial pressure within a range of 70 to 180 mmHg (normal mean
arterial pressure is 100 mmHg). The ability of the kidneys to
maintain a relatively constant GFR in the face of fluctuating
blood pressures is called renal autoregulation.
In renal autoregulation, afferent arterioles dilate when the
mean arterial pressure falls toward 70 mmHg and constrict
when the mean arterial pressure rises above normal. Changes

Figure 17.11 Sympathetic nerve effects. The effect

of increased sympathetic nerve activity on kidney function and

other physiological processes is illustrated.

Blood pressure Exercise

Baroreceptor r eflex

Sympathetic

nerve activity

Vasoconstriction

of afferent arterioles

in kidneys

Total

peripheral

GFR resistance

Urine

production

Blood volume

Vasoconstriction

in skin, GI tract

Cardiac

output

Stimuli

Negative feedback corrections

that may occur in the efferent arterioles are believed to be of

secondary importance.

Blood flow to the glomeruli and GFR can thus remain rel-

atively constant within the autoregulatory range of blood pres-

sure values. The effects of different regulatory mechanisms on

the GFR are summarized in table 17.1.

Two general mechanisms are responsible for renal auto-

regulation: (1) myogenic constriction of the afferent arteriole,

due to the ability of the smooth muscle to sense and respond

to an increase in arterial pressure; and (2) the effects of locally

produced chemicals on the afferent arteriole, which is part

of a process called tubuloglomerular feedback. The sensor

in tubuloglomerular feedback is a group of specialized cells

called the macula densa, located in the thick portion of the

ascending limb where it loops back and comes into contact

with the afferent and efferent arterioles in the renal cortex. The

macula densa here is part of a larger functional unit known as

the juxtaglomerular apparatus (see fig. 17.26 ), which will be

described in section 17.5.

When there is an increased delivery of NaCl and H 2 O to the

distal tubule (as occurs when increased arterial pressure causes

a rise in the GFR), the macula densa releases a chemical signal