587
CHAPTER FIFTEEN
Cardiovascular System
Certain chemicals, including carbon dioxide, oxygen,
and hydrogen ions, infl
uence peripheral resistance by affect-
ing precapillary sphincters and smooth muscles in arteriole
and metarteriole walls. For example, increasing blood car-
bon dioxide, decreasing blood oxygen, and lowering of the
blood’s pH relaxes smooth muscle in the systemic circula-
tion. This increases local blood flow to tissues with high
metabolic rates, such as exercising skeletal muscles.
Other chemicals also infl
uence peripheral resistance and
thus blood pressure. Nitric oxide, produced by endothelial
cells, and bradykinin, formed in the blood, are both vaso-
dilators. Angiotensin plays a role in vasoconstriction; and
endothelin, released by cells of the endothelium, is a power-
ful vasoconstrictor. Clinical Application 15.5 discusses high
blood pressure.
PRACTICE
49
What factors aF
ect cardiac output?
50
Explain the ±rank-Starling law of the heart.
51
What is the function of the baroreceptors in the walls of the aortic
arch and carotid sinuses?
52
How does the vasomotor center control peripheral resistance?
Venous Blood Flow
Blood pressure decreases as the blood moves through the
arterial system and into the capillary networks, so little pres-
sure remains at the venular ends of capillaries (see ±
g. 15G).
Instead, blood fl
ow through the venous system is only partly
vasoconstriction increase peripheral resistance, increasing
blood pressure; factors causing vasodilation decrease periph-
eral resistance, decreasing blood pressure.
The
vasomotor center
of the medulla oblongata continu-
ally sends sympathetic impulses to the smooth muscles in the
arteriole walls, keeping them in a state of tonic contraction,
which helps maintain the peripheral resistance associated
with normal blood pressure. The vasomotor center responds
to changes in blood pressure, so it can increase peripheral
resistance by increasing its outfl
ow of sympathetic impulses,
or it can decrease such resistance by decreasing its sympa-
thetic outfl
ow. In the latter case, the vessels vasodilate as
sympathetic stimulation decreases.
Whenever arterial blood pressure suddenly increases,
baroreceptors in the aortic arch and carotid sinuses signal
the vasomotor center, and the sympathetic outfl ow to the
arteriole walls falls
(fig. 15.38)
. The resulting vasodila-
tion decreases peripheral resistance, and blood pressure
decreases toward the normal level.
Similarly, if blood pressure drops, as following a hemor-
rhage, the vasomotor center increases sympathetic outfl
ow.
The resulting release of epinephrine and norepinephrine
vasoconstricts most systemic vessels, increasing peripheral
resistance. This helps return blood pressure toward normal.
The vasomotor center’s control of vasoconstriction and
vasodilation is especially important in the arterioles of the
abdominal viscera
(splanchnic region). These vessels, if fully
dilated, could accept nearly all the blood of the body and send
the arterial pressure toward zero. Thus, control of their diam-
eters is essential in regulating normal peripheral resistance.
Cardiac output increases
Blood pressure rises
Baroreceptors in aortic arch and
carotid sinuses are stimulated
Sensory impulses to cardiac center
Parasympathetic impulses to heart
SA node inhibited
Heart rate decreases
Blood pressure returns
toward normal
FIGURE 15.38
Dilating arterioles helps regulate blood pressure.
FIGURE 15.37
If blood pressure rises, baroreceptors initiate the
cardioinhibitor re²
ex, which lowers the blood pressure.
Rising blood pressure
Stimulation of baroreceptors in
aortic arch and carotid sinuses
Sensory impulses to vasomotor center
Vasomotor center inhibited
Less frequent sympathetic impulses
to arteriole walls
Vasodilation of arterioles
Decreased peripheral resistance
Blood pressure returns toward normal
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