The Endocrine System
343
may develop hypotension, due primarily to a marked decrease
in total peripheral resistance caused by the vasodilators.
As item 3 in Table 11–3 notes, we still do not know the
other reasons, in addition to the effect on vascular smooth
muscle, why increased cortisol is so important for the body’s
optimal response to stress—that is, for its ability to resist the
damaging infl uences of stress. What is clear is that a person
exposed to severe stress can die, usually of circulatory failure,
if his or her plasma cortisol concentration is too low.
Effect 4 in Table 11–3 stems originally from the fact that
administration of large amounts of cortisol or its synthetic
analogs profoundly reduces the infl ammatory response to
injury or infection. Because of this effect, cortisol is a valu-
able tool in the treatment of
allergy,
arthritis,
other infl
am-
matory diseases, and graft rejection. These anti-infl
ammatory
and anti-immune effects have generally been classifi ed among
the various
pharmacological
effects of cortisol because it was
assumed they could be achieved only by very large doses. It
is now clear, however, that such effects also occur, albeit to
a lesser degree, at the plasma concentrations achieved during
stress. Thus, the increased plasma cortisol typical of infection
or trauma exerts a dampening effect on the body’s immune
responses, protecting against possible damage from excessive
infl ammation. This effect explains the signifi cance of the fact,
mentioned earlier, that several cytokines (immune cell secre-
tions) stimulate the secretion of ACTH and thereby cortisol.
Such stimulation is part of a negative feedback system in which
the increased cortisol then partially blocks the infl
ammatory
processes in which the cytokines participate. Moreover, corti-
sol normally dampens the fever an infection causes.
In summary, stress is a broadly defi ned situation in
which there exists a real or potential threat to homeostasis.
In such a scenario, it is important to maintain blood pressure,
to provide extra fuel sources in the blood, and to temporarily
shut down nonessential functions. Cortisol is the most impor-
tant hormone that carries out these activities. Thus, cortisol
enhances vascular reactivity, catabolizes protein and fat to pro-
vide energy, and inhibits growth and reproduction. The price
the body pays during stress is that cortisol is strongly cata-
bolic. Thus, cells of the immune system, bone, muscles, skin,
and numerous other tissues undergo catabolism to provide
substrates for gluconeogenesis. In the short term, this is not of
any major consequence. Chronic exposure to stress, however,
can in fact lead to severe decreases in bone density, immune
function, and reproductive fertility.
Other Hormones Released
During Stress
Other hormones that are usually released during many kinds of
stress are aldosterone, vasopressin (ADH), growth hormone,
glucagon, and beta-endorphin (which is coreleased from the
anterior pituitary with ACTH). Insulin secretion usually
decreases. Vasopressin and aldosterone act to retain water and
sodium within the body, an important adaptation in the face
of potential losses by hemorrhage or sweating. Vasopressin also
stimulates the secretion of ACTH. The overall effects of the
changes in growth hormone, glucagon, and insulin are, like
those of cortisol and epinephrine, to mobilize energy stores.
The role, if any, of beta-endorphin in stress may be related to
its painkilling effects.
In addition, the sympathetic nervous system plays a key
role in the stress response. Activation of the sympathetic ner-
vous system during stress is often termed the
ght-or-fl
ight
response.
A list of the major effects of increased sympathetic
activity, including secretion of epinephrine from the adrenal
medulla, almost constitutes a guide to how to meet emergen-
cies in which physical activity may be required and bodily
damage may occur (
Table 11–4
).
Table 11–3
Effects of Increased Plasma Cortisol
Concentration During Stress
1. Effects on organic metabolism
a. Stimulation of protein catabolism in bone, lymph,
muscle, and elsewhere
b. Stimulation of liver uptake of amino acids and their
conversion to glucose (gluconeogenesis)
c. Maintenance of plasma glucose levels
d. Stimulation of triglyceride catabolism in adipose tissue,
with release of glycerol and fatty acids into the blood
2. Enhanced vascular reactivity (increased ability to maintain
vasoconstriction in response to norepinephrine and other
stimuli)
3. Unidentifi ed protective effects against the damaging
infl uences of stress
4. Inhibition of infl
ammation and specifi c immune responses
5. Inhibition of nonessential functions (e.g., reproduction and
growth)
Table 11–4
Actions of the Sympathetic Nervous
System, Including Epinephrine Secreted
by the Adrenal Medulla, During Stress
1. Increased hepatic and muscle glycogenolysis (provides a
quick source of glucose)
2. Increased breakdown of adipose tissue triglyceride (provides
a supply of glycerol for gluconeogenesis and of fatty acids for
oxidation)
3. Decreased fatigue of skeletal muscle
4. Increased cardiac function (e.g., increased heart rate)
5. Diversion of blood from viscera to skeletal muscles by means
of vasoconstriction in the former beds and vasodilation in
the latter
6. Increased lung ventilation by stimulating brain breathing
centers and dilating airways
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