C h a p t e r 1 8
Disorders of Blood Flow and Blood Pressure
423
Diastolic Pressure.
The diastolic
blood pressure reflects the closure of the
aortic valve, the energy that has been
stored in the elastic fibers of the large
arteries during systole, and the resis-
tance to flow through arterioles into the
capillaries. Closure of the aortic valve
at the onset of diastole and recoil of the
elastic fibers in the aorta and large arter-
ies continue to drive the blood forward,
even though the heart is not pumping.
These effects, largely restricted to the
elastic vessels, convert the discontinu-
ous systolic flow in the ascending aorta
into a continuous flow in the peripheral
arteries.
Peripheral
resistance
Diastolic
240
220
200
180
160
140
120
100
80
60
40
20
250
230
210
170
150
130
110
90
70
50
30
10
Aorta
Left
atrium
Left
ventricle
3
with cardiovascular centers in the brain stem and
can induce widespread vasoconstriction. Whenever
the arterial pressure drops below a critical level, the
chemoreceptors are stimulated because of diminished
oxygen supply and a buildup of carbon dioxide and
hydrogen ions. In persons with chronic lung disease,
systemic and pulmonary hypertension may develop
because of hypoxemia (see Chapter 23). Persons with
sleep apnea may also experience an increase in blood
pressure because of the hypoxemia that occurs during
the apneic periods.
Humoral Mechanisms.
The
humoral control
of blood
pressure relies on a number of mechanisms, including
the
renin-angiotensin-aldosterone
system and
vasopres-
sin.
26
Other humoral substances, such as epinephrine, a
sympathetic neurotransmitter released from the adrenal
gland, have the effect of directly producing an increase
in heart rate, cardiac contractility, and vascular tone.
The
renin-angiotensin-aldosterone system
plays a
central role in blood pressure regulation. Renin is an
enzyme that synthesized and stored by the juxtaglo-
merular cells of the kidney and released in response to
an increase in sympathetic nervous system activity or
a decrease in blood pressure, extracellular fluid vol-
ume, or extracellular sodium concentration.
26
Most of
the renin that is released leaves the kidney and enters
the bloodstream, where it acts enzymatically to convert
an inactive circulating plasma protein called
angioten-
sinogen
to angiotensin I (Fig. 18-15). Angiotensin I is
then converted to angiotensin II. This conversion occurs
almost entirely in the small vessels of the lung, catalyzed
by an enzyme called the
angiotensin-converting enzyme
that is present in the endothelium of the lung vessels.
Although angiotensin II has a half-life of only several
minutes, renin persists in the circulation for 30 minutes
to 1 hour and continues to cause production of angio-
tensin II during this time.
Angiotensin II functions in both the short- and long-
term regulation of blood pressure. It is a strong vasocon-
strictor, particularly of arterioles and, to a lesser extent,
of veins. Constriction of the arterioles increases the
peripheral vascular resistance, thereby contributing to
the short-term regulation of blood pressure. Angiotensin
II also reduces sodium excretion by increasing sodium
reabsorption by the proximal tubules of the kidney. A
second major function of angiotensin II, stimulation of
aldosterone secretion from the adrenal gland, contrib-
utes to the long-term regulation of blood pressure by
increasing salt and water retention by the kidney.
Blood Pressure
(
text continued from page 421
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