HORMONAL REGULATION OF STRESS
When
a threat or danger is perceived, the body responds by releasing hormones that
will ready it for the “fight-or-flight” response. The effects of this response
are familiar to anyone who has been in a stressful situation: increased heart
rate, dry mouth, and hair standing up.
FIGHT-OR-FLIGHT
RESPONSE
Interactions of the endocrine
hormones have evolved to ensure the body’s internal environment remains stable.
Stressors are stimuli that disrupt homeostasis. The sympathetic division of the
vertebrate autonomic nervous system has evolved the fight-or-flight response to
counter stress-induced disruptions of homeostasis. In the initial alarm phase,
the sympathetic nervous system stimulates an increase in energy levels through
increased blood glucose levels. This prepares the body for physical activity
that may be required to respond to stress: to either fight for survival or to
flee from danger.
However, some stresses, such as illness or injury, can last
for a long time. Glycogen reserves, which provide energy in the short-term
response to stress, are exhausted after several hours and cannot meet long-term
energy needs. If glycogen reserves were the only energy source available,
neural functioning could not be maintained once the reserves became depleted
due to the nervous system’s high requirement for glucose. In this situation,
the body has evolved a response to counter long-term stress through the actions
of the glucocorticoids, which ensure that long-term energy requirements can be
met. The glucocorticoids mobilize lipid and protein reserves, stimulate
gluconeogenesis, conserve glucose for use by neural tissue, and stimulate the
conservation of salts and water. The mechanisms to maintain homeostasis that
are described here are those observed in the human body. However, the
fight-or-flight response exists in some form in all vertebrates.
The
sympathetic nervous system regulates the stress response via the hypothalamus.
Stressful stimuli cause the hypothalamus to signal the adrenal medulla (which
mediates short-term stress responses) via nerve impulses, and the adrenal
cortex, which mediates long-term stress responses, via the hormone adrenocorticotropic hormone (ACTH),
which is produced by the anterior pituitary.
Short-Term Stress Response
When
presented with a stressful situation, the body responds by calling for the
release of hormones that provide a burst of energy. The hormones epinephrine (also known as
adrenaline) and norepinephrine (also
known as noradrenaline) are released by the adrenal medulla. How do these
hormones provide a burst of energy? Epinephrine and norepinephrine increase
blood glucose levels by stimulating the liver and skeletal muscles to break
down glycogen and by stimulating glucose release by liver cells. Additionally,
these hormones increase oxygen availability to cells by increasing the heart
rate and dilating the bronchioles. The hormones also prioritize body function
by increasing blood supply to essential organs such as the heart, brain, and
skeletal muscles, while restricting blood flow to organs not in immediate need,
such as the skin, digestive system, and kidneys. Epinephrine and norepinephrine
are collectively called catecholamines.
Long-Term Stress Response
Long-term
stress response differs from short-term stress response. The body cannot
sustain the bursts of energy mediated by epinephrine and norepinephrine for
long times. Instead, other hormones come into play. In a long-term stress
response, the hypothalamus triggers the release of ACTH from the anterior
pituitary gland. The adrenal cortex is stimulated by ACTH to release steroid
hormones called corticosteroids.
Corticosteroids turn on transcription of certain genes in the nuclei of target
cells. They change enzyme concentrations in the cytoplasm and affect cellular
metabolism. There are two main corticosteroids: glucocorticoids such as cortisol, and mineralocorticoids
such as aldosterone. These hormones target the breakdown of fat into fatty
acids in the adipose tissue. The fatty acids are released into the bloodstream
for other tissues to use for ATP production. The glucocorticoids
primarily affect glucose metabolism by stimulating glucose synthesis.
Glucocorticoids also have anti-inflammatory properties through inhibition of
the immune system. For example, cortisone is used as an anti-inflammatory
medication; however, it cannot be used long term as it increases susceptibility
to disease due to its immune-suppressing effects.
Mineralocorticoids
function to regulate ion and water balance of the body. The hormone aldosterone
stimulates the reabsorption of water and sodium ions in the kidney, which
results in increased blood pressure and volume.
Hypersecretion
of glucocorticoids can cause a condition known as Cushing’s disease, characterized by a shifting
of fat storage areas of the body. This can cause the accumulation of adipose
tissue in the face and neck, and excessive glucose in the blood. Hyposecretion
of the corticosteroids can cause Addison’s
disease, which may result in bronzing of the skin, hypoglycemia, and low
electrolyte levels in the blood.
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