610
U N I T 7
Kidney and Urinary Tract Function
Two major systems are credited with maintaining the
constancy of renal blood flow and GFR: one responds
to changes in arterial pressure and the other to changes
in the sodium chloride concentration in the distal tubu-
lar fluid. Both serve to regulate the tone of the afferent
arteriole. The pressure sensitive mechanism, termed the
myogenic mechanism
, relies on the intrinsic property
of vascular smooth muscle that causes it to contract
when stretched. Thus, when the arterial pressure rises
and the afferent arteriole is stretched, the smooth mus-
cle contracts; when arterial pressure falls, the smooth
muscle relaxes.
The second mechanism, termed the
tubuloglomerular
feedback mechanism,
involves a feedback loop in which
the sodium chloride concentration in the tubular fluid
is sensed by the
juxtaglomerular apparatus
(“juxta”
meaning “next to”) in the distal tubule. This feedback
system, which is located at the site where the distal
tubule extends back to the glomerulus and then passes
between the afferent and efferent arterioles, includes a
group of sodium sensing cells called the
macula densa
and special secretory cells in the walls of afferent and
efferent arterioles called
juxtaglomerular cells
that syn-
thesize and release the enzyme renin (Fig. 24-11A).
Because of its location between the afferent and effer-
ent arterioles, the juxtaglomerular apparatus is thought
to play an essential feedback role in linking the level
of arterial blood pressure and renal blood flow to the
GFR and the composition of the distal tubular fluid
(see Fig. 24-11B). It is thought to monitor the arterial
blood pressure by sensing both the stretch of the affer-
ent arteriole and the concentration of sodium chloride
in the tubular filtrate as it passes through the macula
densa. This information is then used in determining how
much renin should be released to keep the arterial blood
pressure within its normal range and maintain a rela-
tively constant GFR. A decrease in the GFR, for exam-
ple, increases sodium chloride reabsorption, thereby
decreasing the delivery of sodium chloride to the macula
densa. The decrease in delivery of sodium chloride to
the macula densa has two effects: it decreases resistance
to blood flow in the afferent arteriole, which raises glo-
merular filtration pressure; and it increases the release
of renin from the juxtaglomerular cells. The renin from
these cells functions as an enzyme to convert the plasma
protein angiotensinogen to angiotensin I, which is con-
verted to angiotensin II in the lungs (see Chapter 18,
Fig. 18-12). Angiotensin II acts to constrict the efferent
arteriole as a means of producing a further increase in
the glomerular filtration pressure; thereby returning the
GFR toward a more normal range.
Effects of Increased Protein and Glucose Load
Although renal blood flow and glomerular filtration
are relatively stable under most conditions, two factors
can increase renal blood flow and glomerular filtration:
(1) high protein intake, (2) an increase in blood glu-
cose. With ingestion of a high-protein meal, renal
blood flow increases 20% to 30% within 1 to 2 hours.
FIGURE 24-11.
(A)
Juxtaglomerular apparatus showing the close contact of the distal tubule with
the afferent arteriole, the macula densa, and the juxtaglomerular cells.
(B)
Flow chart depicting
the macula densa feedback mechanism for autoregulation of glomerular hydrostatic pressure and
glomerular filtration rate (GFR) during changes in renal arterial pressure. (From Hall JE. Guyton and
HallTextbook of Medical Physiology. 12th ed. Philadelphia, PA: Saunders Elsevier; 2011:320.)
Glomerulus
Basement
membrane
Afferent
arteriole
Efferent
arteriole
Macula
densa
Distal
tubule
Juxtaglomerular
cells
A
Arterial pressure
Glomerular hydrostatic
pressure
GFR
Macula densa
NaCl
Renin
Angiotensin II
Efferent
arteriolar
resistance
Afferent
arteriolar
resistance
Proximal
NaCl
reabsorption
B
