200
CARDIOVASCULAR PHYSIOLOGY CONCEPTS
Central
Command
Hypothalamus
Muscle and Joint
Afferents
P a r a s y m p a t h e t i c
I n h ib itio n
Medulla
S y m p a t h e t i c
A c t i v a t i o n
r
|
Y
Heart
■<-
Adrenals
Blood Vessels
t
H e a r t r a t e
t I n o t r o p y
t L u s i t r o p y
C a t e c h o l a m i n e
r e l e a s e
A r t e r i a l a n d v e n o u s
c o n s t r i c t i o n
■ FIGURE 9.1 Summary of adrenergic and cholinergic control mechanisms during exercise. The hypothala-
mus functions as an integrative center that receives inform ation from the brain and muscle and joint recep-
tors, then modulates sym pathetic and parasympathetic (vagal) outflow from the medulla. Sym pathetic
nerves are activated leading to cardiac stim ulation, arterial and venous constriction (not in active muscles),
and adrenal release of catecholamines; parasym pathetic inhibition removes vagal tone on the heart.
Sympathetic nerves innervating the adre-
nal medulla cause the secretion of epineph-
rine and lesser amounts of norepinephrine
into the blood (see Chapter 6). Plasma norep-
inephrine concentrations increase more than
10-fold during exercise. A large fraction of
this norepinephrine comes from sympathetic
nerves. Normally, most of the norepineph-
rine released by sympathetic nerves is taken
back up by the nerves (neuronal reuptake);
however, some of the norepinephrine can dif-
fuse (“spillover”) into the capillary blood and
enter the systemic circulation. This spillover
is greatly enhanced when the level of sympa-
thetic activity is high in the body. The blood
transports the epinephrine and norepineph-
rine to the heart and other organs, where these
hormones act upon a- and P-adrenoceptors
to enhance cardiac function and either con-
strict or dilate blood vessels. In Chapter 6,
we learned that epinephrine (at low concen-
trations) binds to P2-adrenoceptors in skel-
etal muscle, which causes vasodilation. At
high concentrations, epinephrine also binds
to postjunctional a 1- and a 2-adrenoceptors
on blood vessels to cause vasoconstriction.
Circulating norepinephrine constricts blood
vessels
by
binding
preferentially
to
a 1-
adrenoceptors in most organs. During exer-
cise, circulating levels of norepinephrine and
epinephrine can become very high so that the
net effect on the vasculature is a-adrenocep-
tor-mediated
vasoconstriction,
except
in
those organs (e.g., heart and active skeletal
muscle) in which metabolic mechanisms pro-
duce vasodilation. It is important to note that
vasoconstriction
produced
by
sympathetic
nerves and circulating catecholamines does
not occur in the active skeletal muscle, coro-
nary circulation, or brain because blood flow
in these organs is primarily controlled by local
metabolic vasodilator mechanisms.
Increased sympathetic activity stimulates
renal release of renin, which leads to the for-
mation of angiotensin II. Increased angio-
tensin II increases renal sodium and water
reabsorption by directly affecting renal func-
tion and by stimulating aldosterone secretion;
in addition, angiotensin II augments sympa-
thetic activity (see Chapter 6). Circulating
arginine vasopressin (antidiuretic hormone)
also increases during exercise, most likely
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