Porth's Essentials of Pathophysiology, 4e - page 627

C h a p t e r 2 4
Structure and Function of the Kidney
609
Peritubular
capillary
Interstitial fluid
Blood
ADH
Basolateral
membrane
Luminal
membrane
Collecting duct
epithelium
Tubular
urine
Aquaporin-2
channels
H
2
O
H
2
O
H
2
O
H
2
O
Cyclic
AMP
ATP
Vasopressin
receptor
Action of ADH.
Antidiuretic hor-
mone, also known as vasopressin,
acts at the level of the collecting
tubule to increase water absorp-
tion. It exerts its action by bind-
ing to vasopressin receptors on the
basolateral membrane of the tubu-
lar cell. Binding of ADH to the
vasopressin receptors causes water
channels (
aquaporin-2 channels
) to
move into the luminal side of the
cell membrane, which is normally
impermeable to water. Insertion of
the channels allows water from the
tubular fluids to move into the tubu-
lar cell and then out into the sur-
rounding hyperosmotic interstitial
fluid on the basolateral side of the
cell. From there it moves into the
peritubular capillaries for return to
the circulatory system. Thus, when
ADH is present, the water that
moved from the blood into the urine
filtrate in the glomeruli is returned
to the circulatory system, and when
ADH is absent, the water is excreted
in the urine.
3
constriction of the afferent and efferent arterioles and
thus a decrease in renal blood flow. Intense sympathetic
stimulation such as occurs in shock and trauma can pro-
duce marked decreases in renal blood flow and GFR,
even causing blood flow to cease altogether.
Several humoral substances, including angiotensin II,
ADH, and the endothelins, produce vasoconstriction of
renal vessels. The endothelins are a group of peptides
released from damaged endothelial cells in the kid-
ney and other tissues. Although not thought to be an
important regulator of renal blood flow during everyday
activities, endothelin I may play a role in the reduction
of blood flow in conditions such as postischemic renal
failure (see Chapter 26).
Other substances such as dopamine, nitric oxide,
and prostaglandins (i.e., E
2
and I
2
) produce vasodi-
lation. Nitric oxide, a vasodilator produced by the
vascular endothelium, appears to be important in pre-
venting excessive vasoconstriction of renal blood vessels
and allowing normal excretion of sodium and water.
Prostaglandins are a group of mediators of cell func-
tion that are produced locally and exert their effects
locally. Prostaglandins do not appear to play a major
role in regulating renal blood flow and GFR under
normal conditions, but may protect the kidneys against
the vasoconstricting effects of sympathetic stimulation
and angiotensin II. This effect is important because it
prevents severe and potentially harmful vasoconstric-
tion and ischemia during conditions such as hemorrhage
and shock. Aspirin and other nonsteroidal anti-inflam-
matory drugs (NSAIDs) that inhibit prostaglandin syn-
thesis may decrease renal blood flow and GFR under
certain conditions.
Autoregulatory Mechanisms
The constancy of blood flow through body tissues is
maintained by a process called
autoregulation.
In most
tissues other than the kidneys, autoregulation functions
to maintain blood flow at a level consistent with the
metabolic needs of the tissues. In the kidney, autoregula-
tion of blood flow also functions to maintain a relatively
constant GFR and to allow for the precise regulation of
solute and water excretion.
Concentrates Urine
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text continued from page 607
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