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• Two systems coordinate communication
throughout the body: the endocrine system and
the nervous system
• The endocrine system secretes hormones
that coordinate slower but longer-acting
responses including reproduction,
development, energy metabolism, growth, and
behavior
• The nervous system conveys high-speed
electrical signals along specialized cells called
neurons; these signals regulate other cells
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
In multicellular animals, nerve impulses provide electric
signals; hormones provide chemical signals.
Hormones are secreted by cells, diffuse into the
extracellular fluid, and often are distributed by the
circulatory system. Hormones reach all parts of the
body, but only target cells are equipped to respond
Hormones work much more slowly than nerve impulse
transmission and are not useful for controlling rapid
actions.
Hormones coordinate longer-term developmental
processes such as reproductive cycles.
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Concept 45.1: Hormones and other signaling
molecules bind to target receptors, triggering
specific response pathways
• Signals can be of many kinds light, sound,
smell, touch etc. many of which are due to
chemicals.
• Chemical signals bind to receptor proteins on
target cells
• Only target cells with the appropriate receptor
respond to the signal
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Types of Secreted Signaling Molecules
• Secreted chemical signals include
– Hormones
– Local regulators
– Neurotransmitters
– Neurohormones
– Pheromones
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Local Regulators
• Local regulators are chemical signals that
travel over short distances by diffusion
• Local regulators help regulate blood pressure,
nervous system function, and reproduction
• Local regulators are divided into two types
– Paracrine signals act on cells near the
secreting cell
– Autocrine signals act on the secreting cell
itself
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Signaling by Local Regulators
• In paracrine signaling, nonhormonal chemical
signals called local regulators elicit responses
in nearby target cells
• Types of local regulators:
– Cytokines and growth factors
– Nitric oxide (NO)
– Prostaglandins
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• Long distance signaling involves the chemical
being taken by circulation to the target tissues.
Usually hormones are released from a special
cell or organ called an endocrine cell/organ,
travel through the bloodstream, and interact
with the receptor or a target cell to cause a
physiological response.
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Fig. 45-2
Blood
vessel
Response
(a) Endocrine signaling
Response
(b) Paracrine signaling
Response
(c) Autocrine signaling
Synapse
Neuron
Response
(d) Synaptic signaling
Neurosecretory
cell
Blood
vessel
(e) Neuroendocrine signaling
Response
Chemical Classes of Hormones
• Three major classes of molecules function as
hormones in vertebrates:
– Polypeptides (proteins and peptides)
– Amines derived from amino acids
– Steroid hormones
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• Lipid-soluble hormones (steroid hormones)
pass easily through cell membranes, while
water-soluble hormones (polypeptides and
amines) do not
• The solubility of a hormone correlates with the
location of receptors inside or on the surface of
target cells
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Fig. 45-3
Water-soluble
Lipid-soluble
0.8 nm
Polypeptide:
Insulin
Steroid:
Cortisol
Amine:
Epinephrine
Amine:
Thyroxine
Cellular Response Pathways
• Water and lipid soluble hormones differ in their
paths through a body
• Water-soluble hormones are secreted by
exocytosis, travel freely in the bloodstream,
and bind to cell-surface receptors
• Lipid-soluble hormones diffuse across cell
membranes, travel in the bloodstream bound to
transport proteins, and diffuse through the
membrane of target cells
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• Signaling by any of these hormones involves
three key events:
– Reception
– Signal transduction
– Response
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Fig. 45-5-1
Fat-soluble
hormone
Watersoluble
hormone
Signal receptor
Transport
protein
TARGET
CELL
(a)
Signal
receptor
NUCLEUS
(b)
Fig. 45-5-2
Fat-soluble
hormone
Watersoluble
hormone
Transport
protein
Signal receptor
TARGET
CELL
Cytoplasmic
response
OR
Signal
receptor
Gene
regulation
Cytoplasmic
response
(a)
NUCLEUS
(b)
Gene
regulation
Pathway for Water-Soluble Hormones
• Binding of a hormone to its receptor initiates a
signal transduction pathway leading to
responses in the cytoplasm, enzyme activation,
or a change in gene expression
Animation: Water-Soluble Hormone
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Multiple Effects of Hormones
• The same hormone may have different effects
on target cells that have
– Different receptors for the hormone
– Different signal transduction pathways
– Different proteins for carrying out the response
• A hormone can also have different effects in
different species
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Fig. 45-8-1
Same receptors but different
intracellular proteins (not shown)
Epinephrine
Epinephrine
 receptor
 receptor
Glycogen
deposits
Glycogen
breaks down
and glucose
is released.
(a) Liver cell
Vessel
dilates.
(b) Skeletal muscle
blood vessel
Fig. 45-8-2
Same receptors but different
intracellular proteins (not shown)
Different receptors
Epinephrine
Epinephrine
Epinephrine
 receptor
 receptor
 receptor
Glycogen
deposits
Glycogen
breaks down
and glucose
is released.
(a) Liver cell
Vessel
dilates.
(b) Skeletal muscle
blood vessel
Vessel
constricts.
(c) Intestinal blood
vessel
Hormones
• Endocrine signals (hormones) are secreted into
extracellular fluids and travel via the bloodstream
• Endocrine glands are ductless and secrete
hormones directly into surrounding fluid
• Hormones mediate responses to environmental
stimuli and regulate growth, development, and
reproduction
Exocrine glands have ducts and secrete
substances onto body surfaces or into body
cavities (for example, tear ducts)
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Fig. 45-10
Major endocrine glands:
Hypothalamus
Pineal gland
Pituitary gland
Thyroid gland
Parathyroid glands
Organs containing
endocrine cells:
Thymus
Heart
Adrenal
glands
Testes
Liver
Stomach
Pancreas
Kidney
Kidney
Small
intestine
Ovaries
Concept 45.2: Negative feedback and antagonistic
hormone pairs are common features of the
endocrine system
• Hormones are assembled into regulatory
pathways
• A negative feedback loop inhibits a response
by reducing the initial stimulus
• Negative feedback regulates many hormonal
pathways involved in homeostasis
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Coordination of Endocrine and Nervous Systems
in Invertebrates
• In insects, molting and development are
controlled by a combination of hormones:
– A brain hormone stimulates release of
ecdysone from the prothoracic glands
– Juvenile hormone promotes retention of larval
characteristics
– Ecdysone promotes molting (in the presence of
juvenile hormone) and development (in the
absence of juvenile hormone) of adult
characteristics
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Fig. 45-13-3
Brain
Neurosecretory cells
Corpus cardiacum
PTTH
Corpus allatum
Low
JH
Prothoracic
gland
Ecdysone
EARLY
LARVA
Juvenile
hormone
(JH)
LATER
LARVA
PUPA
ADULT
Coordination of Endocrine and Nervous Systems
in Vertebrates
• The hypothalamus receives information from
the nervous system and initiates responses
through the endocrine system
• Attached to the hypothalamus is the pituitary
gland composed of the posterior pituitary and
anterior pituitary
The pituitary gland of mammals is a link between the
nervous system and many endocrine glands and
plays a crucial role in the endocrine system.
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Fig. 45-14
Cerebrum
Pineal
gland
Thalamus
Cerebellum
Pituitary
gland
Hypothalamus
Spinal cord
Hypothalamus
Posterior
pituitary
Anterior
pituitary
• The posterior pituitary stores and secretes
hormones that are made in the
hypothalamus:these hormones are called
neuroendocrine hormones
• The anterior pituitary makes and releases
hormones under regulation of the
hypothalamus
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Fig. 45-15
Hypothalamus
Neurosecretory
cells of the
hypothalamus
Axon
Posterior
pituitary
Anterior
pituitary
HORMONE
ADH
Oxytocin
TARGET
Kidney tubules
Mammary glands,
uterine muscles
ADH
The function of antidiuretic hormone (ADH) is to
increase water conservation by the kidney.
If there is a high level of ADH secretion, the
kidneys resorb water.
If there is a low level of ADH secretion, the
kidneys release water in dilute urine.
ADH release by the posterior pituitary increases if
blood pressure falls or blood becomes too salty.
ADH causes peripheral blood vessel constriction
to help elevate blood pressure and is also
called vasopressin.
• Oxytocin induces uterine contractions and the
release of milk
• Suckling sends a message to the
hypothalamus via the nervous system to
release oxytocin, which further stimulates the
milk glands
• This is an example of positive feedback,
where the stimulus leads to an even greater
response
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Fig. 45-17
Tropic effects only:
FSH
LH
TSH
ACTH
Neurosecretory cells
of the hypothalamus
Nontropic effects only:
Prolactin
MSH
Nontropic and tropic effects:
GH
Hypothalamic
releasing and
inhibiting
hormones
Portal vessels
Endocrine cells of
the anterior pituitary
Posterior pituitary
Pituitary hormones
HORMONE
FSH and LH
TSH
ACTH
Prolactin
MSH
GH
TARGET
Testes or
ovaries
Thyroid
Adrenal
cortex
Mammary
glands
Melanocytes
Liver, bones,
other tissues
Tropic Hormones
• A tropic hormone regulates the function of
endocrine cells or glands
• The four strictly tropic hormones are
– Thyroid-stimulating hormone (TSH)
– Follicle-stimulating hormone (FSH)
– Luteinizing hormone (LH)
– Adrenocorticotropic hormone (ACTH)
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Nontropic Hormones
• Nontropic hormones target nonendocrine tissues
• Nontropic hormones produced by the anterior
pituitary are
– Prolactin (PRL)
– Melanocyte-stimulating hormone (MSH)
• Prolactin stimulates lactation in mammals but has
diverse effects in different vertebrates
• MSH influences skin pigmentation in some
vertebrates and fat metabolism in mammals
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Growth Hormone
• Growth hormone (GH) is secreted by the
anterior pituitary gland and has tropic and
nontropic actions
• It promotes growth directly and has diverse
metabolic effects
• It stimulates production of growth factors
• An excess of GH can cause gigantism, while a
lack of GH can cause dwarfism
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Figure 42.6 Effects of Excess Growth Hormone
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Releasing and Release inhibiting Neurohormones
of the Hypothalumus
Anterior Pituitary Hormones
• Hormone production in the anterior pituitary is
controlled by releasing and inhibiting hormones
from the hypothalamus
• For example, the production of thyrotropin
releasing hormone (TRH) in the hypothalamus
stimulates secretion of the thyroid stimulating
hormone (TSH) from the anterior pituitary
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Hormone Cascade Pathways
• A hormone can stimulate the release of a
series of other hormones, the last of which
activates a nonendocrine target cell; this is
called a hormone cascade pathway
• The release of thyroid hormone results from a
hormone cascade pathway involving the
hypothalamus, anterior pituitary, and thyroid
gland
• Hormone cascade pathways are usually
regulated by negative feedback
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Fig. 45-18-3
Pathway
Example
Stimulus
Cold
Sensory
neuron
–
Hypothalamus secretes
thyrotropin-releasing
hormone (TRH )
Neurosecretory
cell
Blood
vessel
–
Negative feedback
Anterior pituitary secretes
thyroid-stimulating
hormone (TSH
or thyrotropin )
Thyroid gland secretes
thyroid hormone
(T3 and T4 )
Target
cells
Response
Body tissues
Increased cellular
metabolism
Thyroid Hormone: Control of Metabolism and
Development
• The thyroid gland consists of two lobes on the
ventral surface of the trachea
• It produces two iodine-containing hormones:
triiodothyronine (T3) and thyroxine (T4)
Two forms of thyroxine, T3 and T4, are made from
tyrosine. T3 (triiodothyronine) has three iodine
atoms. T4 has four iodine atoms.
More T4 is produced in thyroid, but it can be converted
to T3 by an enzyme in the blood. T3 is the more
active form of the hormone.
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Thyroxine has many roles in regulating metabolism.
It stimulates the transcription of many genes in nearly all
cells in the body. These include genes for enzymes of
energy pathways, transport proteins, and structural
proteins.
It elevates metabolic rates in most cells and tissues.
It promotes the use of carbohydrates over fats for fuel.
It promotes amino acid uptake and protein synthesis and
so is critical for metabolism, growth and development.
Insufficient thyroxine may result in cretinism.
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• Hyperthyroidism, excessive secretion of thyroid
hormones, causes high body temperature,
weight loss, irritability, and high blood pressure
• Hypothyroidism, low secretion of thyroid
hormones, causes weight gain, lethargy, and
intolerance to cold
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• A goiter is an enlarged thyroid gland associated with either
very low (hypothyroidism) or very high (hyperthyroidism)
levels of thyroxine.
Hyperthyroid goiter results when the negative feedback
mechanism fails even though blood levels of thyroxine are high.
A common cause is an autoimmune disease in which an antibody
to the TSH receptor is produced. This antibody binds the TSH
receptor, causing the thyroid cells to release excess thyroxine.
(Graves’ disease)
The thyroid remains maximally active and grows larger, causing
symptoms associated with high metabolic rates.
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Hypothalamus
Anterior
pituitary
TSH
Thyroid
T3 + T4
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Hypothyroid goiter results when there is insufficient
thyroxine to turn off TSH production.
The most common cause is a deficiency of dietary
iodine.
With high TSH levels, the thyroid gland continues to
produce nonfunctional thyroxine and becomes
very large.
The body symptoms of this condition are low
metabolism, cold intolerance, and physical and
mental sluggishness.
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Parathyroid Hormone and Vitamin D: Control of
Blood Calcium
• Two antagonistic hormones regulate the
homeostasis of calcium (Ca2+) in the blood of
mammals
– Parathyroid hormone (PTH) is released by
the parathyroid glands
– Calcitonin is released by the thyroid gland
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Vertebrate Endocrine Systems- Calcium regulation
Calcium levels in the blood must be regulated within a
narrow range. Small changes in blood calcium levels
have serious effects.
Most calcium in the body is in the bones (99%). About
1% is in the cells, and only 0.1% is in the extracellular
fluids.
Blood calcium levels are regulated by:
Deposition and absorption of bone
Excretion of calcium by the kidneys
Absorption of calcium from the digestive tract
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Hormonal control of calcium homeostasis in
mammals
Thyroid gland
releases
calcitonin.
Calcitonin
Reduces
Ca2+ uptake
in kidneys
Stimulates
Ca2+ deposition
in bones
Blood Ca2+
level declines
to set point
STIMULUS:
Rising blood
Ca2+ level
Homeostasis:
Blood Ca2+ level
(about 10 mg/100 mL)
STIMULUS:
Falling blood
Ca2+ level
Blood Ca2+
level rises
to set point
Stimulates
Ca2+ release
from bones
Parathyroid
gland
PTH
Increases
Ca2+ uptake
in intestines
Active
vitamin D
Stimulates Ca2+
uptake in kidneys
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Vertebrate Endocrine Systems
Calcitonin, released by the thyroid gland, acts to
lower calcium levels in the blood.
Bone is constantly remodeled by absorption of old
bone and production of new bone.
Osteoclasts break down bone and release calcium.
Osteoblasts use circulating calcium to build new
bone.
Calcitonin decreases osteoclast activity and
stimulates the osteoblasts to take up calcium for
bone growth.
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Vertebrate Endocrine Systems
Blood calcium decrease triggers release of parathyroid
hormone (PTH), from the parathyroid glands which
are embedded in the posterior surface of the thyroid
gland.
This in turn causes the osteoclasts to dissolve bone and
release calcium.
Parathyroid hormone also promotes calcium resorption
by the kidney to prevent loss in the urine.
It also promotes vitamin D activation, which stimulates
the gut to absorb calcium from food.
Parathyroid hormone and calcitonin act antagonistically
to regulate blood calcium levels.
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Vertebrate Endocrine Systems
In the kidneys, vitamin D acts with PTH to decrease
calcium loss in urine.
In bone vitamin D acts like PTH to stimulate bone
turnover and the liberation of calcium
The overall action of vitamin D is to raise blood
calcium levels, which promotes bone deposition.
Vitamin D also acts in a negative feedback loop to
inhibit transcription of the PTH gene in the
parathyroid glands.
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Vertebrate Endocrine Systems
Bone minerals have both calcium and phosphate.
When PTH stimulates the release of calcium from bone,
phosphate is also released.
Normal levels of calcium and phosphate in the blood are
close to the concentration that could cause them to
precipitate as calcium phosphate salts.
Calcium phosphate salts are involved in the formation of
kidney stones and hardening of artery walls.
PTH acts on the kidneys to increase the elimination of
phosphate to reduce the possibility of calcium
phosphate salt precipitation.
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Vertebrate Endocrine Systems –Glucose Regulation
Insulin and glucagon are antagonistic hormones that help
maintain glucose homeostasis
Insulin is produced in the pancreas in cell clusters called islets of
Langerhans.
Several cell types have been identified in the islets:
Beta () cells produce and secrete insulin.
Alpha () cells produce and secrete glucagon (antagonist of
insulin).
Delta (d) cells produce somatostatin.
The remainder of the pancreas acts as an exocrine gland with
digestive functions.
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Vertebrate Endocrine Systems
After a meal, blood glucose levels rise and stimulate
the  cells to release insulin.
Insulin stimulates cells to use glucose and to convert
it to glycogen and fat.
When blood glucose levels fall, the pancreas stops
releasing insulin, and cells switch to using
glycogen and fat for energy.
If blood glucose falls too low, the  cells release
glucagon which stimulates the liver to convert
glycogen back to glucose.
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Maintenance of glucose homeostasis
Body cells
take up more
glucose.
Insulin
Beta cells of
pancreas are stimulated
to release insulin
into the blood.
Liver takes
up glucose
and stores it
as glycogen.
STIMULUS:
Rising blood glucose
level (for instance, after
eating a carbohydraterich meal)
Blood glucose level
declines to set point;
stimulus for insulin
release diminishes.
Homeostasis:
Blood glucose level
(about 90 mg/100 mL)
Blood glucose level
rises to set point;
stimulus for glucagon
release diminishes.
STIMULUS:
Dropping blood glucose
level (for instance, after
skipping a meal)
Alpha cells of pancreas
are stimulated to release
glucagon into the blood.
Liver breaks
down glycogen
and releases
glucose into
blood.
Glucagon
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Target Tissues for Insulin and Glucagon
• Insulin reduces blood glucose levels by
– Promoting the cellular uptake of glucose
– Slowing glycogen breakdown in the liver
– Promoting fat storage
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• Glucagon increases blood glucose levels by
– Stimulating conversion of glycogen to glucose
in the liver
– Stimulating breakdown of fat and protein into
glucose
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Vertebrate Endocrine Systems
Diabetes mellitus is a disease caused by a lack of
the protein hormone insulin (Type I) or a lack of
insulin receptors on target cells (Type II).
Insulin binds to receptors on the cell membrane and
allows glucose uptake.
Without insulin or the receptors, glucose
accumulates in the blood until it is lost in urine.
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Vertebrate Endocrine Systems
High glucose levels in the blood cause water to
move from the cells into the blood by osmosis.
The kidneys then increase urine output to get rid of
the fluid excess.
Cells not taking up glucose use fat and protein for
fuel, resulting in the body’s wasting away and
tissue and organ damage.
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Adrenal Hormones: Response to Stress
• The adrenal glands are adjacent to the kidneys
• Each adrenal gland actually consists of two glands: the
adrenal medulla (inner portion) and adrenal cortex (outer
portion)
The medulla produces epinephrine and norepinephrine.
The medulla develops from the nervous system and remains
under its control.
The cortex is under hormonal control, mainly by
adrenocorticotropin (ACTH) from the anterior pituitary.
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Catecholamines from the Adrenal Medulla
• The adrenal medulla secretes epinephrine
(adrenaline) and norepinephrine
(noradrenaline)
• These hormones are members of a class of
compounds called catecholamines
• They are secreted in response to stressactivated impulses from the nervous system
• They mediate various fight-or-flight responses
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• Epinephrine and norepinephrine
– Trigger the release of glucose and fatty acids
into the blood
– Increase oxygen delivery to body cells
– Direct blood toward heart, brain, and skeletal
muscles, and away from skin, digestive
system, and kidneys
• The release of epinephrine and norepinephrine
occurs in response to nerve signals from the
hypothalamus
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Vertebrate Endocrine Systems
Epinephrine and norepinephrine are amine hormones.
They bind to two types of receptors in target cells: adrenergic and -adrenergic
Norepinephrine acts mostly on the alpha type, so
drugs called beta blockers, which inactivate only adrenergic receptors, can be used to reduce fight-orflight responses to epinephrine.
The beta blockers leave the alpha sites open to
norepinephrine and its regulatory functions.
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Fig. 45-21
Stress
Spinal cord
Nerve
signals
Hypothalamus
Releasing
hormone
Nerve
cell
Anterior pituitary
Blood vessel
ACTH
Adrenal medulla
Adrenal cortex
Adrenal
gland
Kidney
(a) Short-term stress response
Effects of epinephrine and norepinephrine:
1. Glycogen broken down to glucose; increased blood glucose
2. Increased blood pressure
3. Increased breathing rate
4. Increased metabolic rate
5. Change in blood flow patterns, leading to increased
alertness and decreased digestive, excretory, and
reproductive system activity
(b) Long-term stress response
Effects of
mineralocorticoids:
Effects of
glucocorticoids:
1. Retention of sodium 1. Proteins and fats broken down
ions and water by
and converted to glucose, leading
kidneys
to increased blood glucose
2. Increased blood
volume and blood
pressure
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2. Possible suppression of
immune system
Fig. 45-21b
Adrenal medulla
Adrenal
gland
Kidney
(a) Short-term stress response
Effects of epinephrine and norepinephrine:
1. Glycogen broken down to glucose; increased blood glucose
2. Increased blood pressure
3. Increased breathing rate
4. Increased metabolic rate
5. Change in blood flow patterns, leading to increased
alertness and decreased digestive, excretory, and
reproductive system activity
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Fig. 45-21c
Adrenal cortex
Adrenal
gland
Kidney
(b) Long-term stress response
Effects of
mineralocorticoids:
Effects of
glucocorticoids:
1. Retention of sodium
ions and water by
kidneys
1. Proteins and fats broken down
and converted to glucose, leading
to increased blood glucose
2. Increased blood
volume and blood
pressure
2. Possible suppression of
immune system
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Vertebrate Endocrine Systems
Adrenal cortex cells use cholesterol to produce three
classes of steroid hormones called corticosteroids:
Glucocorticoids influence blood glucose
concentrations and other aspects of fuel
molecule metabolism.
Mineralocorticoids influence extracellular ionic
balance.
Sex steroids stimulate sexual development and
reproductive activity. These are secreted in only
minimal amounts by the adrenal cortex.
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Figure 42.11 The Corticosteroid Hormones are Built from Cholesterol
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Vertebrate Endocrine Systems
The main mineralocorticoid, aldosterone, stimulates
the kidney to conserve sodium and excrete
potassium.
The main glucocorticoid, cortisol, mediates the
body’s response to stress.
The fight-or-flight response ensures that muscles
have adequate oxygen and glucose for immediate
response.
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Vertebrate Endocrine Systems
Shortly after a frightening stimulus, blood cortisol
rises.
Cortisol stimulates cells that are not critical to the
emergency to decrease their use of glucose.
It also blocks the immune system reactions, which
temporarily are less critical.
Cortisol can therefore be used to reduce
inflammation and allergy.
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Vertebrate Endocrine Systems
Cortisol release is controlled by ACTH from the
anterior pituitary which, in turn is controlled by
adrenocorticotropin-releasing hormone from
the hypothalamus.
The cortisol response is much slower than the
epinephrine response.
Turning off the cortisol response is also critical to
avoid the consequences of long-term stress.
Cortisol has negative feedback effect on brain cells
that decreases the release of adrenocorticotropinreleasing hormone.
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Vertebrate Endocrine Systems- Reproduction
The gonads (testes and ovaries) produce steroid
hormones synthesized from cholesterol.
Androgens are male steroids, the dominant one being
testosterone.
Estrogens and progesterone are female steroids, the
dominant estrogen being estradiol.
Sex steroids determine whether a fetus develops into a
male or female.
After birth, sex steroids control maturation of sex organs
and secondary sex characteristics such as breasts
and facial hair.
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Vertebrate Endocrine Systems
Until the seventh week of an embryo’s development,
either sex may develop.
In mammals, the Y chromosome causes the gonads to
start producing androgens in the seven-week-old
embryo, and the male reproductive system develops.
If androgens are not released, the female reproductive
system develops.
In birds, the opposite rules apply: male features are
produced unless estrogens are present to trigger
female development.
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Vertebrate Endocrine Systems
Sex steroid production increases rapidly at puberty, or
sexual maturation, in humans.
Control of sex steroids (both male and female) is under
the anterior pituitary tropic hormones called
luteinizing hormone (LH) and follicle-stimulating
hormone (FSH).
These gonadotropins are controlled by the
hypothalamic gonadotropin-releasing hormone
(GnRH).
Before puberty, the hypothalamus produces low levels of
GnRH.
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Vertebrate Endocrine Systems
At puberty GnRH release increases, stimulating
gonadotropin production and, hence, sex steroid
production.
In females, increased LH and FSH at puberty induce
the ovaries to begin female sex hormone
production to initiate sexually mature body traits.
In males, increased LH stimulates cells in the testes
to make androgens which induce changes
associated with adolescence.
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Vertebrate Endocrine Systems
Synthetic androgens (anabolic steroids) can
exaggerate body strength and muscle development.
Negative side effects in females include more masculine
body features, such as shrinking the uterus and
causing an irregular menstrual cycle.
In males, the negative side effects include shrinking of
the testes, enlarged breasts, and sterility.
Continued use of anabolic steroids may increase risk of
heart disease, some cancers, kidney damage, and
personality disorders.
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Melatonin and Biorhythms
• The pineal gland, located in the brain,
secretes melatonin
• Light/dark cycles control release of melatonin
• Primary functions of melatonin appear to relate
to biological rhythms associated with
reproduction
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Vertebrate Endocrine Systems
Many other body organs, such as the gut and the
heart, produce hormones.
When blood pressure stretches the heart wall, its
cells release atrial natriuretic hormone.
This hormone increases sodium ion and water
excretion by the kidney, lowering blood pressure
and blood volume.
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Hormone Actions:
The Role of Signal Transduction Pathways
Hormones are released in very small amounts, yet
they cause large and very specific responses in
target organs and tissues.
Strength of hormone action results from signal
transduction cascades that amplify the original
signal.
Selective action is keyed to appropriate receptors of
cells responding to hormones.
Specific receptors can also be linked to different
response mechanisms, as is the case with receptors
for epinephrine and norepinephrine.
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Hormone Actions:
The Role of Signal Transduction Pathways
The abundance of hormone receptors can be under
feedback control.
Continuous high levels of a hormone can decrease
the number of its receptors, a process called
downregulation.
High levels of insulin in type II diabetes mellitus
result in a loss of insulin receptors.
Upregulation of receptors is a positive feedback
mechanism and is less common than
downregulation.
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Figure 42.16 Dose-Response Curves Quantify
Response to a Hormone
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Hormone Actions:
The Role of Signal Transduction Pathways
Anything that changes the responsiveness of a
system to a hormone is reflected in the dose–
response curve. These may include:
The number of receptors in the responding cells
Changes in signaling pathways
Changes in rate-limiting enzymes
The availability of substrates or cofactors
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Hormone Actions:
The Role of Signal Transduction Pathways
Hormone responses may also vary in their time course.
The length of time for the concentration of a hormone to
drop to one-half of the maximum is called its half-life.
Epinephrine’s half-life in the blood is only 1–3 minutes.
Cortisol or thyroxine half-lives are on the order of
days.
Half-life is partially determined by degradation and
elimination processes.
Most hormones are broken down in the liver, removed
from the blood by the kidney, and excreted in the
urine.
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Table 45-1b
Table 45-1c
Table 45-1d
You should now be able to:
1. Distinguish between the following pairs of terms:
hormones and local regulators, paracrine and
autocrine signals
2. Describe the evidence that steroid hormones have
intracellular receptors, while water-soluble hormones
have cell-surface receptors
3. Explain how the body regulates general metabolism,
Glucose and Calcium homeostatis.
4. How does the body responds to long tern stress?
5. Distinguish between hypothyroid and hyperthyroid
goitre
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1.
Explain how the hypothalamus and the pituitary glands interact
and how they coordinate the endocrine system
2.
Explain the role of tropic hormones in coordinating endocrine
signaling throughout the body
3.
List and describe the functions of hormones released by the
following: anterior and posterior pituitary lobes, thyroid glands,
parathyroid glands, adrenal medulla, adrenal cortex, gonads,
pineal gland.
4.
Explain how these hormones are regulated.
5.
Explain the general mechanisms of hormone action.
6.
Distinguish signaling by the nervous system vs. the endocrine
system
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