Transmission in
ANS(Catecholamines)
Dr Asma Jabeen
Assistant professor, Physiology
Learning Objectives
At the end of this session, the student should be able to:
•List the sites of release of norepinephrine as a chemical
•transmitter.
•Diagram the steps of catecholamines synthesis.
•Describe the actions of norepinephrine and classify the
•adrenergic receptors according to these actions.
•Describe the removal of norepinephrine.
Transmitters of ANS
Acetylcholine -- para -sympathetic
transmitter.
 Nor epinephrine – sympathetic
transmitter.

Adrenergic fibers:
Most of the postganglionic sympathetic
neurons are adrenergic .
Function of Adrenal medulla:
80% Epinephrine
20% Norepinephrine
 Effects of circulating epinephrine and
Norepinephrine last 5 to 10 times longer
than direct sympathetic stimulation.(2 to
4 min, after stimulation is over.
 Both the hormones are removed from blood slowly
Importance of adrenal medulla as a part
of Sympathetic NS
 The dual mechanism of sympathetic
stimulation ,direct and indirect, provides
a safety factor, one mechanism
substituting for the other if it is missing.
 Epinephrine and norepinephrine can
stimulate structures that are not directly
innervated by sympathetic fibers. e.g.
metabolic rate of every cell is increased.
Difference in action of Epinephrine and
Norepinephrine

Epinephrine has greater effect on
cardiac stimulation (ß-receptors)

Norepinephrine causes stronger
constriction of muscle blood vessels.
Thus it greatly increases TPR and
elevates arterial pressure.

Epinephrine has 5 to 10 times greater
metabolic effect.
Synthesis and removal of Nor epinephrine
Synthesis begins in axoplasm ,completed
in secretary vesicle.
hydroxylation
1.
Tyrosine
2.
Dopa
3.
Dopa
decarboxylation
Dopamine
Transport into vesicle
Hydroxylation
4.
Dopamine
Norepinephrine
In adrenal medulla,
methylation
5.
Nor epinephrine
Removal:
1. Reuptake
2. Diffusion
3. Destruction
Epinephrine
Sites of Synthesis
EpinephrineProduced exclusively in adrenal medulla with a small amount in
the brain. Essentially all the circulating epinephrine is derived
from adrenal medulla.
NorepinephrineIt is widely distributed in neural tissues including the adrenal
medulla, sympathetic post-ganglionic fibers and the central
nervous system. In brain its concentration is highest in the
hypothalamus
Metabolism: Removal and Inactivation
The plasma half life of catecholamine is 1-3 minutes. The biological
effects of catecholamine is terminated rapidly by following two
processes
1. Neuronal uptake (non enzymatic inactivation)
This is presynaptic reuptake accounts for inactivation of about 85%
of released NE. It is less pecific for Ep than for NE
2. Extraneuronal uptake (enzymatic inactivation)
It is mediated by postsynaptic cells and is followed by intracellular
metabolic inactivation. The enzymes involved are mono amine
oxidase (MAO) and catechol-o-methyl transferase (COMT)
Mechanism of action:
The transmitter binds with specific
receptor on the effector cells
 Receptor is on outside of a protein molecule
that penetrates the membrane.
 This causes a conformational change
in protein molecule


Altered protein molecule excite or inhibit the cell
by:


Change of cell membrane
permeability
Activating or inactivating an enzyme
e.g. Adenyle cyclase → CAMP
Adrenergic Receptors:
1.
2.
Alpha receptors
(Alpha 1 and Alpha 2)
Beta receptors
(Beta 1 and Beta 2)
α-Adrenergic Receptors
α-Adrenergic Receptors are sensitive to both Ep and NE
These receptors are again of two types
i. α-1 receptors-located on post synaptic membranes and are
mainly excitatory, e.g. in blood vessels and non pregnant uterus
ii. α-2 receptors- located on presynaptic nerve terminals of
cholinergic and adrenergic nerves. Activation of neuronal α-2
receptors is inhibitory
β-adrenergic receptors
These receptors respond to Ep and in general are relatively insensitive to NE.
These are associated with most of the inhibitory function of the body with
one most important function i.e. excitation of myocardium. There are
following three types of β adrenergic receptors
i. β-1: cardiac muscle
ii. β-2:skeletal muscle blood vessel, GIT and bronchioles
iii. β-3:adipose tissue
Adrenergic receptors in the sympathetic system
b
a1
Norepinephrine
a2
Norepinephrine
Neuroscience, Sinauer Asssoc., Inc
Functions of Alpha Receptors:
•
•
•
•
•
•
Vasoconstriction
Iris dilation
Intestinal relaxation
Intestinal sphincter contraction
Pilomotor contraction
Bladder sphincter contraction
Functions of Beta Receptors:
•
•
•
•
•
•
•
•
•
•
Vasodilation ß2
Cardioacceleration ß1
Increased myocardial strength ß1
Intestinal relaxation ß2
Uterus relaxation ß2
Bronchodilation ß2
Calorigenesis ß2
Glycogenolysis ß2
Lipolysis ß2
Bladder wall relaxation ß2
Location of specific adrenergic receptors
α1 receptors
•vascular smooth muscle, on GI and bladder sphincters,
and radial muscle of the eye
•causes excitation (contraction)
α2 receptors
•presynaptic nerve terminals, platelets, fat cells, walls
of GI tract
•causes inhibition (relaxation, dilation)
β1 receptors
•SA node, AV node, ventricular muscle of
heart
• Produces excitation, increases heart rate,
contractility, and conduction velocity
β2 receptors
•Vascular smooth muscle of skeletal muscle,
bronchioles, walls of GI tract and bladder
•Produces relaxation: dilation of vascular
smooth muscle and relaxation of bladder,
bronchioles
Sympathetic Action and
Receptors at Target Organs
Organ
Action
Heart
heart rate
contactility
AV node conduction
Vascular smooth
Muscle
differential effects!
constrict blood vessels
(dilates blood vessel
in skeletal muscles)
Gastrointestinal
Tract
motility
constricts sphincters
Receptor
b1
a1
b2
a2, b2
b2
Bronchioles
dilates bronchiolar
smooth muscle
Males sex organs
ejaculation
a
Bladder
relaxes bladder wall
constricts sphincter
b2
a
Sympathetic Action Cont…d
organ
action
receptor
sweat glands
sweating
goose bumps
skin
kidney
contracts
blood flow
renin secretion
a1
fat cells
lipolysis
b1
pupil
dilation
a1
salivary
glands
secretion
a/b
muscarinic
b1
Thank you