Page 1029 - Fundamentals of anatomy physiology
P. 1029
1016 Unit 5 Environmental Exchange
not excreted, pH control is jeopardized, and an important juxtaglomerular complex. Renin converts the inactive protein
mechanism for regulating blood volume is lost. It should be angiotensinogen to angiotensin I. Angiotensin I is also inactive
no surprise that a variety of regulatory mechanisms ensure that but is then converted to angiotensin II by angiotensin-con-
GFR remains within normal limits. verting enzyme (ACE). This conversion takes place primarily
in the capillaries of the lungs. Angiotensin II acts at the neph-
Filtration depends on adequate blood flow to the glom- ron, adrenal glands, and in the CNS. In peripheral capillary
erulus and on the maintenance of normal filtration pressures. beds, angiotensin II causes a brief but powerful vasoconstric-
Three interacting levels of control stabilize GFR: (1) autoregula- tion of arterioles and precapillary sphincters, increasing arte-
tion, at the local level; (2) hormonal regulation, initiated by the rial pressures throughout the body. The combined effect is an
kidneys; and (3) autonomic regulation, primarily by the sympa- increase in systemic blood volume and blood pressure and the
thetic division of the autonomic nervous system. restoration of normal GFR.
Autoregulation of the GFR If blood volume increases, the GFR increases automati-
cally. This increase promotes fluid losses that help return blood
Autoregulation (local blood flow regulation) maintains an ad- volume to normal levels. If the increase in blood volume is
equate GFR despite changes in local blood pressure and blood severe, hormonal factors further increase the GFR and speed
flow. Myogenic mechanisms—how arteries and arterioles react up fluid losses in the urine. As noted in Chapter 18, the heart
to an increase or decrease in blood pressure—play a role in releases natriuretic peptides when increased blood volume or
the autoregulation of blood flow. Changes to the diameters blood pressure stretches the walls of the heart. The atria release
of afferent arterioles, efferent arterioles, and glomerular capil- atrial natriuretic peptide (ANP), and the ventricles release brain
laries maintain GFR. The most important regulatory mecha- natriuretic peptide (BNP). pp. 666, 775 Among their other
nisms stabilize the GFR when systemic blood pressure drops effects, these hormones trigger the dilation of afferent arterioles
(Figure 26–11). and the constriction of efferent arterioles. This mechanism
increases glomerular pressures and increases the GFR. The na-
The GFR also remains relatively constant when systemic triuretic peptides also decrease sodium reabsorption at the
blood pressure increases. An increase in renal blood pressure renal tubules. The net result is increased urine production and
stretches the walls of afferent arterioles, and the smooth muscle decreased blood volume and pressure.
cells respond by contracting. The reduction in the diameter of
afferent arterioles decreases glomerular blood flow and keeps Autonomic Regulation of the GFR
the GFR within normal limits.
Most of the autonomic innervation of the kidneys consists
26 Hormonal Regulation of the GFR of sympathetic postganglionic fibers. (The role of the few para-
sympathetic fibers in regulating kidney function is not known.)
The GFR is regulated by the hormones of the renin–angiotensin- Sympathetic activation has a direct effect on the GFR. It pro-
aldosterone system and the natriuretic peptides (ANP and duces a powerful vasoconstriction of afferent arterioles, which
BNP). We introduced these hormones and their actions in decreases the GFR and slows the production of filtrate. In this
Chapters 18 and 21. pp. 665–667, 772–775 There are three way, the sympathetic activation triggered by an acute decrease
triggers for the release of renin by the juxtaglomerular complex in blood pressure or a heart attack overrides the local regulatory
(JGC). They are (1) a decrease in blood pressure at the glom- mechanisms that act to stabilize the GFR. As the crisis passes
erulus as the result of a decrease in blood volume, a decrease and sympathetic tone decreases, the filtration rate gradually
in systemic pressures, or a blockage in the renal artery or its returns to normal.
branches; (2) stimulation of juxtaglomerular cells by sympa-
thetic innervation; or (3) a decrease in the osmotic concentra- When the sympathetic division alters regional patterns of
tion of the tubular fluid at the macula densa. blood circulation, blood flow to the kidneys is often affected.
For example, the dilation of superficial vessels in warm weather
These triggers are often interrelated. For example, a de- shunts blood away from the kidneys. As a result, glomerular
crease in systemic blood pressure reduces the glomerular filtra- filtration decreases temporarily. The effect becomes especially
tion rate, while baroreceptor reflexes cause sympathetic activa- pronounced during strenuous exercise. As the blood flow to
tion. Meanwhile, a decrease in the GFR slows the movement of your skin and skeletal muscles increases, kidney perfusion grad-
tubular fluid along the nephron. As a result, the tubular fluid ually decreases. These changes may be opposed, with variable
is in the ascending limb of the nephron loop longer, and the success, by autoregulation at the local level.
concentration of sodium and chloride ions in the tubular fluid
reaching the macula densa and DCT becomes abnormally low. At maximal levels of exertion, renal blood flow may be less
than 25 percent of normal resting levels. This reduction can cre-
Figure 26–11 provides a general overview of the response ate problems for endurance athletes. Metabolic wastes build up
of the renin–angiotensin-aldosterone system to a decrease in
GFR. A decrease in GFR leads to the release of renin by the
