Chapter 19
The Cardiovascular System: Blood Vessels
707
19
hypothalamus also mediates the redistribution of blood flow
and other cardiovascular responses that occur during exercise
and changes in body temperature.
Short-Term Regulation: Hormonal Controls
Hormones also help regulate blood pressure, both in the short
term via changes in peripheral resistance and in the long term
via changes in blood volume
(Table 19.2)
. Paracrines (local
chemicals), on the other hand, primarily serve to match blood
flow to the metabolic need of a particular tissue. In rare in-
stances, massive release of paracrines can affect blood pressure.
We will discuss these paracrines later—here we will examine the
short-term effects of hormones.
Adrenal medulla hormones.
During periods of stress, the
adrenal gland releases
epinephrine
and
norepinephrine
(NE)
to the blood. Both hormones enhance the sympathetic
response by increasing cardiac output and promoting gener-
alized vasoconstriction.
Angiotensin II.
When blood pressure or blood volume are
low, the kidneys release renin. Renin acts as an enzyme, ul-
timately generating
angiotensin II
(an
0
je-o-ten
9
sin), which
stimulates intense vasoconstriction, promoting a rapid rise
in systemic blood pressure. It also stimulates release of aldos-
terone and ADH, which act in long-term regulation of blood
pressure by enhancing blood volume.
Atrial natriuretic peptide (ANP).
Te atria of the heart pro-
duce the hormone
atrial natriuretic peptide (ANP)
, which
leads to a reduction in blood volume and blood pressure.
As noted in Chapter 16, ANP antagonizes aldosterone and
prods the kidneys to excrete more sodium and water from
the body, reducing blood volume. It also causes generalized
vasodilation.
Antidiuretic hormone (ADH).
Produced by the hypotha-
lamus,
antidiuretic hormone
(
ADH
, also called
vaso-
pressin
) stimulates the kidneys to conserve water. It is not
usually important in short-term blood pressure regulation.
However, when blood pressure falls to dangerously low lev-
els (as during severe hemorrhage), much more ADH is re-
leased and helps restore arterial pressure by causing intense
vasoconstriction.
In the opposite situation, a decline in MAP initiates reflex
vasoconstriction and increases cardiac output, bringing blood
pressure back up. In this way, peripheral resistance and cardiac
output are regulated in tandem to minimize changes in blood
pressure.
Rapidly responding baroreceptors protect the circulation
against short-term (acute) changes in blood pressure. For ex-
ample, blood pressure falls (particularly in the head) when
you stand up a±er reclining. Baroreceptors taking part in the
carotid sinus reflex
protect the blood supply to your brain,
whereas those activated in the
aortic reflex
help maintain ad-
equate blood pressure in your systemic circuit as a whole.
Baroreceptors are relatively
ineffective
in protecting us
against sustained pressure changes, as evidenced by the fact that
many people develop chronic hypertension. In such cases, the
baroreceptors are “reprogrammed” (adapt) to monitor pressure
changes at a higher set point.
Chemoreceptor Reflexes
When the carbon dioxide levels rise, or the pH falls, or oxygen
content of the blood drops sharply,
chemoreceptors
in the aor-
tic arch and large arteries of the neck transmit impulses to the
cardioacceleratory center, which then increases cardiac output,
and to the vasomotor center, which causes reflex vasoconstric-
tion. Te rise in blood pressure that follows speeds the return of
blood to the heart and lungs.
Te most prominent chemoreceptors are the
carotid
and
aortic bodies
located close by the baroreceptors in the carotid
sinuses and aortic arch. Chemoreceptors play a larger role in
regulating respiratory rate than blood pressure, so we consider
their function in Chapter 22.
Influence of Higher Brain Centers
Reflexes that regulate blood pressure are integrated in the me-
dulla oblongata of the brain stem. Although the cerebral cortex
and hypothalamus are not involved in routine controls of blood
pressure, these higher brain centers can modify arterial pressure
via relays to the medullary centers.
For example, the fight-or-flight response mediated by the
hypothalamus has profound effects on blood pressure. (Even
the simple act of speaking can make your blood pressure
jump if the person you are talking to makes you anxious.) Te
Table 19.2
Effects of Selected Hormones on Blood Pressure
HORMONE
EFFECT ON BP
VARIABLE AFFECTED
SITE OF ACTION
Epinephrine and norepinephrine (NE)
CO (HR and contractility)
Peripheral resistance (vasoconstriction)
Heart (
b
1
receptors)
Arterioles (
a
receptors)
Angiotensin II
Peripheral resistance (vasoconstriction)
Arterioles
Atrial natriuretic peptide (ANP)
Peripheral resistance (vasodilation)
Arterioles
Antidiuretic hormone (ADH)
Peripheral resistance (vasoconstriction)
Blood volume (
water loss)
Arterioles
Kidney tubule cells
Aldosterone
Blood volume (
water and salt loss)
Kidney tubule cells
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