Physiology
ENDOCRINE SYSTEM
Edited by:
Dr. Gholamreza Komeili
Comparison of Nervous and
Endocrine Systems
Nervous
Endocrine
messenger
electrochemical
hormone
(chemical)
response
milliseconds
seconds to days
duration
short-lived
long-lived
one system (several
distribution
subsystems)
widely scattered
NOTE: Nervous and endocrine systems work together to
coordinate and integrate activities of body (homeostasis)
Functions of Endocrine System
1. Reproduction
2. Growth and development
3. Response to stress
4. Maintenance of fluid (water), electrolyte and
nutrient balance
5. Regulation of cellular metabolism and energy
Organs of the Endocrine System
1. Pituitary gland
2. Hypothalamus (neuroendocrine)
3. Pineal gland
4. Thyroid gland
5. Parathyroid gland
6. Thymus gland
7. Adrenal gland
8. Pancreas (also has exocrine function)
9. Gonads (testes or ovaries - also have exocrine functions)
Topics
• Hormone
– Types
– Modes of Action
– Target cell activation
– Control
• Specific glands, their hormones, and disorders
– Pituitary
– Thyroid
– Parathyroid
– Adrenal
– Pancreas
– Thymus
– Gonads (testes and ovaries)
• General Adaptation Syndrome
• chemicals
Hormones
• secreted by endocrine gland cells into blood (by way of
interstitial fluid)
• regulate metabolic functions of other cells (called target
cells)
• carried to all cells, but action is specific to cells that have
receptors for the hormone
– specificity of body’s response to hormone depends on
how many cells have the receptor (highly specific if few
cells respond [e.g., ACTH]; diffuse action if many respond
[e.g., thyroxin])
Chemical Types of Hormones
• Amino-acid based (amino acids, short or long peptides,
proteins)
– e.g., insulin, growth hormone, prolactin
• Steroids - lipid derivatives of cholesterol
– e.g., hormones from gonads (testosterone, estrogen)
– e.g., hormones from adrenal cortex (adrenocortical
hormones)
• Eicosanoids - locally-secreted, locally-acting hormones
secreted by all cell membranes (e.g., prostaglandins,
which increase blood pressure and contribute to uterine
contraction)
Types of Changes in Target Cells
• plasma membrane permeability changes (opening of
protein channels; may change membrane potential)
• activation of genes for increased protein synthesis,
including enzymes
• activation or deactivation of enzymes already present
• secretion of cellular products
• stimulation of cell division (mitosis)
Mechanisms of Action
• action in target cell depends on receptor
• receptor may be:
– in plasma membrane
• second messenger mechanisms
• used by most amino acid-based hormones (water
soluble)
– intracellular (in cytoplasm or nucleus)
• direct gene activation
• used by steroids and thyroid hormones (lipid
soluble)
Mechanisms of Action: Steroids
• bind to intracellular receptors
• hormone diffuses through plasma membrane and makes
its way to nucleus
– > where it binds with intracellular receptor to form
hormone-receptor complex
– > hormone-receptor complex interacts with chromatin
(DNA) to affect gene activity (turn genes on or off)
– > synthesis of mRNA
– > synthesis of protein
Steroid Signaling
Mechanism of Action:
Thyroid Hormone
• similar to mechanism for steroid hormones
• diffuses across plasma membrane
– diffuses into nucleus where it interacts with
intracellular receptors to activate genes for proteins
(enzymes) involved in cellular respiration (glycolysis)
– also, binds to receptors at mitochondria to activate
genes for proteins involved in cellular respiration
(Krebs cycle and electron transport chain)
Mechanisms of Action:
Other Hormones
* plasma membrane receptor
• used by most amino acid-based hormones
• interaction of hormone with plasma membrane receptor
results in activation of second messenger systems (cyclic
AMP or PIP-calcium)
• activation of second messenger has cascade effect
resulting in:
– enzyme activation, or
– membrane permeability changes or secretion
Membrane Receptor Mechanisms:
1. Cyclic AMP (cAMP) Signaling
• interaction of hormone with receptor
– > activates G protein (cleaves phosphate from GTP)->
excitation
– > G protein activates adenylate cyclase
– > adenylate cyclase forms cAMP from ATP
– > cAMP activates protein kinases
– > protein kinases activate (or inhibit) other proteins by
phosphorylation
– > cAMP degraded by enzyme
• slightly different G protein inactivates adenylate cyclase associated with different hormone receptor
• Link to animation:
http://student.ccbc.cc.md.us/c_anatomy/animat/cAMP.htm
cAMP Signaling Mechanism
Membrane Receptor Mechanisms:
2. PIP-Calcium Signaling
• interaction of hormone with receptor --> activates
membrane-bound enzyme phospholipase
– > phospholipase cleaves PIP2 (phosphatidyl inositol
diphosphate) into diacylglycerol (DAG) and IP3 -- each
of which acts as a second messenger
• diacylglycerol (DAG) activates protein kinases
• IP3 (inositol triphosphate) causes release of Ca2+
into cytoplasm (from endoplasmic reticulum or
other storage areas) --> Ca2+ acts as third messenger
PIP-Calcium Mechanism (con’t)
-> Ca2+ (third messenger)
– changes enzyme activity and plasma membrane
channels, or
– binds to calmodulin (intracellular regulatory
protein) --> activates enzymes
– see Fig. 17.2 for examples of proteins that act
through membrane-receptors and 2nd
messengers
PIP-Calcium Signaling Mechanism
Factors Affecting Target Cell
Activation
a. blood levels of hormone, which depend on:
– rate of hormone release
– rate of deactivation (by target cell or liver)
b. affinity of hormone for receptor
– greater affinity means greater association --> greater
effect
c. number of receptors available
Factors Affecting Target Cell
Activation (con’t)
c. number of receptors available
– up-regulation: increase in blood level of specific hormone
(normally present at low levels) causes cells to make more
receptors
– down-regulation: prolonged exposure to high level of
specific hormone --> cells remove some receptors
-->return to normal response level
– cross-regulation: influence of one hormone on number of
receptors for another hormone; e.g., progesterone causes
uterus to make fewer estrogen receptors; estrogen causes
uterus to make more progesterone receptors
Hormone Removal
• hormones may be:
– degraded by specific enzymes within target cells;
– removed from blood by kidneys (excreted in urine)
– degraded by liver (excreted in urine and feces)
• half-life - time for 1/2 of hormone to be removed (from a
fraction of a minute to 30 minutes)
• onset - time from release to action (minutes [amino acidbased] to days [steroids])
• duration of action - how long the effects last (~20 minutes
to several hours)
Control of Hormone Release
• Humoral control
• Neural control
• Hormonal control
Control of Hormone Release:
Humoral
Hormone released in response to changing blood
levels of ion or nutrient (negative feedback)
parathyroid glands: detects
low blood Ca2+  PTH 
raises blood Ca2
thyroid (Para follicular cells)
detect high blood Ca2+->calcitonin -->decrease
blood Ca2+
Control of Hormone Release:
Humoral
Other examples:
• pancreas:
– beta cells detect high blood glucose  insulin  decreases
blood glucose
– alpha cells detect low blood glucose glucagon  raises
blood glucose
• zona glomerulosa (of adrenal cortex) detects low blood Na+ or
high blood K+  aldosterone ,  K+
Control of Hormone Release: Neural
Hormone released in response to nerve impulse
preganglionic fibers of
sympathetic division
 stimulate release
of catecholamines
(epinephrine,
norepinephrine)
from adrenal
medulla
impulses from
hypothalamus result
in release of oxytocin
or ADH from
posterior pituitary
Control of Hormone Release:
Hormonal
Hormone produced by one endocrine gland (or hypothalamus)
affects secretion of hormone by another endocrine gland
• hypothalamus acts as overall coordinator  releases
regulatory hormones (releasing hormones or inhibitory
hormones)  affects anterior pituitary
• anterior pituitary, when stimulated, secretes hormones that
affect other glands (e.g., TSH [thyroid stimulating hormone]
stimulates release of thyroid hormones from thyroid gland)
Hormone Control - Misc.
• nervous system can override normal endocrine control
– e.g., in “fight-or-flight” response, sympathetic impulses
result in release of epinephrine and norepinephrine from
adrenal medulla --> increases blood glucose levels to
maintain fuel supply during stress or exertion (overrules
effect of insulin on blood glucose level)