FAR

EASTERN UNIVERSITY – NICANOR REYES MEDICAL FOUNDATION

Physiology A
Gloria Marie M. Valerio, MD
AUTONOMICS
NERVOUS SYSTEM
↙ ↘
CENTRAL NERVOUS SYSTEM PERIPHERAL NERVOUS SYSTEM
(Sensory) toward the brain (Motor) away from the brain
↙ ↘ ↙ ↘
BRAIN SPINAL CORD SOMATIC NS AUTONOMIC / VISCERAL NS
☛Sympathetic NS
☛Parasympathetic NS
☛Enteric NS
☛Brain 
 ☛Ganglia 

STRUCTURES OF THE ☛Spinal Cord 
 ☛Enteric Plexus 

NERVOUS SYSTEM ☛Cranial Nerves 
 ☛Sensory Receptors 

☛Spinal Nerves 

PERIPHERAL NERVOUS 1. 12 pairs Cranial Nerves and its branches (originating from the brain stem) 

SYSTEM 2. 31 pairs Spinal Nerves and its branches (originating from the segments of the spinal cord) 

1. Brain 

CENTRAL NERVOUS SYSTEM
2. Spinal Cord 

Oh Oh Oh To Touch And Feel A Girl’s Vagina Ah Heaven!
Some Say Marry Money, But My Brother Said Big Boobs Matter Most.
CN I – Olfactory Sensory
CN II – Optic Sensory
CN III – Oculomotor Motor
CN IV – Trochlear Motor
CN V – Trigeminal Both
CRANIAL NERVES
CN VI – Abducens Motor

CN VII – Facial Both
CN VIII – Vestibulocochlear Sensory
CN IX – Glossopharyngeal Both
CN X – Vagus Both
CN XI – Accessory Motor
CN XII – Hypoglossal Motor
*CN that are part of ANS: III, VII, IX, X
Cervical Nerves C1-C8 Cervical Plexus
Brachial Plexus
SPINAL NERVES
Thoracic Nerves T1-T12 Intercostal/ Thoracic Nerves

Subcostal nerve
*Thoracic, Lumbar, Sacral
Lumbar Nerves L1-L5 Lumbar Plexus
Nerves are part of ANS
Sacral Nerves S1-S5
Sacral Plexus
Coccygeal Nerves/ Roots
SOMATIC NERVE SYSTEM
1. Somatic Afferent
Sensory receptors (Head, Body Wall, Extremities) → Center
2. Somatic Efferent
NERVE FIBERS Center → Effector cells (Skeletal Muscle)
PERIPHERAL NERVOUS
SYSTEM (SNS + ANS) VISCERAL NERVE/ AUTONOMIC SYSTEM
3. Visceral Afferent
Sensory receptors (Internal Organs) → Center
4. Visceral Efferent
Center → Effector cell (Visceral smooth, Cardiac, Glands)
Sensory receptors 1. Mechanoreceptors (ex. intestinal walls, stretching of walls because of retained food) 

specialized structures located 2. Thermoreceptors (ex. skin, changes in temperature) 

in almost all parts of the body, 3. Photoreceptors (ex. eyes, changes in the wavelength of light) 

stimulated by changes 4. Chemoreceptors (ex. mouth, chemical composition of food) 

inside/outside the body 5. Baroreceptors (ex. blood vessels, arterial wall is stretched during BP increase) 

6. Nociceptors (ex. Free nerve endings – for pain) 


SOURCES:
• Dra. Valerio’s discussion and presentation




FAR EASTERN UNIVERSITY – NICANOR REYES MEDICAL FOUNDATION
Physiology A
Gloria Marie M. Valerio, MD
AUTONOMICS
Sensory receptors (+)
Receptor potential – local potential generated by sensory receptors when stimulated 

If threshold voltage, Local Potential → Action Potential (AP) → Sensory impulse (SI)
Located in all parts stimulated by changes in & out of body
↓
Afferent Nerve (Sensory Nerve)
Transmits AP/SI to the center
↓
REFLEX ARC Center (Brain and Spinal Cord)
The center will analyze the sensory impulse, and then generate a motor impulse

↓
Efferent Nerve (Motor Nerve)
Motor impulse will be transmitted by efferent nerve to the different effector cells/organs 

↓
Effector Cells (4 Types)
Effector cells perform the function, as dictated by the motor impulse. 

Skeletal Muscle, Cardiac Muscle, Smooth Muscle, Glands (↑↓ secretion)

DIFFERENCE SOMATIC NERVOUS SYSTEM AUTONOMIC NERVOUS SYSTEM

Subconscious/ Involuntary/ Automatic
Reflexes Conscious/ Voluntary / Deliberate Response Note: mostly involuntary but some are partly
voluntary (respiration, micturition, defecation)
Orients individual to the external environment Regulates the internal environment
Function
Brings about movement/ locomotion Regulates Visceral Function/ Homeostasis
Head, Body Wall, Extremities Viscera (internal organs)
☛Somatic senses (tactile, thermal, pain and ☛Associated with interoceptors (sensory receptors
Sensory Receptors/ Input 
proprioceptive sensations) and 
 in blood vessels, visceral organs, muscles and
☛Special senses (vision, hearing, taste, smell 
and nervous system) that monitor conditions in the
equilibrium) 
 internal environment.
Main: Cerebral Cortex
Center Hypothalamus, Brain Stem, Spinal Cord
Others: Basal ganglia, Cerebellum, Spinal Cord
Effector/ Organ Skeletal Muscle Visceral Smooth, Cardiac, Glands
Two Neuron Fiber
Center ⎯⎯⎯˂ Ganglion⎯⎯⎯˂ Effector Cell
One Neuron Fiber

Effector Nerve Center ⎯⎯⎯⎯⎯⎯⎯⎯⎯⎯⎯˂ Effector Cell
Ganglions: Neuron found outside brain/SC
(α motor neuron) (Skeletal Muscle)
B – small myelinated (Pre-ganglionic)
C – Small unmyelinated (Post-ganglionic)
Neurotransmitter/s Utilized Acetylcholine (Ach) Acetylcholine (Ach), Norepinephrine (NE)
Center, Peripheral Ganglion,
Sites of Inhibition Center, Neuromuscular Junction (NMJ)
Neuroeffector Junctions (NEJ)
Automaticity – generates own AP
Interruption (cut nerves) No Contraction → Complete paralysis → Atrophy (Automatic Cell) Maintains activity
spontaneously independent of stimulation.
Leads to EXCITATION OR INHIBITION
of the effector cells
☛Smooth Muscle: Contraction/ Relaxation
Always leads to EXCITATION of the muscles
Excitation / Inhibition ☛Cardiac: Increased or Decreased rate and force
(Contraction of the skeletal muscles)
of contraction
☛Glands: Increased or Decreased secretion of
glands

Subdivisions of Autonomic NS ☛Sympathetic (SNS) ☛Parasympathetic (PSNS) ☛Enteric (NS)
1. GIT has its own nervous system 

2. Neurons lie in the GIT wall (esophagus tanus):
Myenteric or Auerbach Plexus – GIT motor (Motility, Peristalsis)
Meissner’s plexus/ Submucosal Layer – regulates secretory activity of GIT 

Enteric Nervous System 3. Can regulate activities GIT activities but ENTERIC activities are regulated by SNS and PNS. 

4. SYMPA postganglionic fibers will synapse with GIT neurons. Indirectly innervates the organs of the GIT.
SYMPA stimulation will decrease GIT motor and secretory activities.
PARASYMPA preganglionic fibers that will synapse with the Enteric NS (like a peripheral ganglion).
PARASYMPA stimulation will increase GIT motor and secretory activities.

SOURCES:
• Dra. Valerio’s discussion and presentation




FAR EASTERN UNIVERSITY – NICANOR REYES MEDICAL FOUNDATION
Physiology A
Gloria Marie M. Valerio, MD
AUTONOMICS
Sympathetic Postganglionic Fibers ↓ENS ↓ GI Motor / Secretory Activity
(Inhibitory) Effect: CONSTIPATION
Parasympathetic Preganglionic ↑ENS ↑ GI Motor/ Secretory Activity
Fibers (Excitation) Effect: DIARRHEA

AUTONOMICAL DIFFERENCES
DIFFERENCE SYMPATHETIC NERVOUS SYSTEM (SNS) PARASYMPATHETIC NERVOUS SYSTEM (PSNS)
CRANIOSACRAL DIVISION
THORACOLUMBAR DIVISION
Originate from brain stem
T1-T2 Head and Neck CN3 Sphincter pupillae/ ciliary
Radial muscle of Iris, Salivary glands CN7 Nasal/ Lacrimal/ Submandibular
T3-T5 Thoracic Region CN9 Protid
Heart, Lungs, Bronchi CN10 Vagus Major Para Nerve
Pre-ganglionic origin
T6-T12 Abdomen Heart, Lungs Bronchi, Lower esophagus, Stomach, Small
and Innervations
Stomach, Small Intestine, Pancreas, Liver, Proximal Half intestine, Proximal half Large Intestine, Pancreas, Liver,
Large Intestine Biliary System Biliary System
L1-L3 Pelvic
Distal Half Large Intestine, Rectum, Anus, Genitourinary Originate from spinal cord
S2 – S4 (Pelvic Nerves)
T1-L3 sweat glands & blood vessels Distal Half L.I., Rectum, Anus, Genitourinary System

TERMINAL GANGLIA

A. Ganglia far from center, near the effector cells
•III Oculomotor: ciliary ganglion: smooth muscle 
of
SYMPATHETIC AND PREVERTEBRAL GANGLIA
Near the center and far from effector cells the eye 

☛sympathetic chain - 22 pairs of ganglion 
 •VII Facial:
(beside vertebral column: paravertebral location) ☛pterigopalatine ganglion: nasal & lacrimal glands
Superior cervical ganglion 
 ☛Submandibular ganglion: submandibular glands
Middle cervical ganglion 
 •IX Glossopharyngeal: otic ganglion: parotid glands

Stellate ganglion 

Location of Peripheral ganglion B. Ganglia far from center or inside effector cell
☛collateral ganglia -3 pairs of ganglion
•X Vagus, Sacral parasympathetic nerves (pelvic
Abdominal/pelvic region, in front of vertebral column:
nerves)
prevertebral
a. Vagus nerve:
Celiac ganglion 

☛Thoracic cavity (heart, lungs, bronchi) 

Superior mesenteric 

☛Abdomen (Esophagus, stomach, small
Inferior mesenteric 


intestine, proximal half of the large


intestine, Liver, pancreas, gall bladder) 

b. Pelvic nerves: Distal half of large intestine,
rectum, anus, genitourinary system
Center ⎯⎯⎯˂ Ganglion⎯⎯⎯⎯⎯⎯⎯⎯⎯⎯˂ Effector Cell Center ⎯⎯⎯⎯⎯⎯⎯⎯⎯⎯˂ Ganglion ⎯⎯⎯˂ Effector Cell
Length Short Pre; Long Post Long Pre; Short or No Post
Preganglionic < Postganglionic Preganglionic > Postganglionic
Extensive branching “Mass Discharge” Limited branching 

Branching of Preganglionic fibers
1 Pre:20post 
 1Pre:1Post 


Sympathetic effects are more widespread and 
diffuse PS Effects are more localized except vagus nerve 


BIOCHEMICAL DIFFERENCES

Acetylcholine – Cholinergic Transmission
Neurotransmitters
Norepinephrine – Noradrenergic / Adrenergic Transmission

Somatic Nervous System Autonomic Nervous System
Locations where NTAs are Somatic Efferent: NMJ Autonomic Efferent: region of PG and NEJ
released somatic nerve terminal autonomic pre- & post-ganglionic nerve ending
Center ⎯⎯⎯⎯⎯⎯⎯⎯⎯⎯⎯⎯⎯⎯⎯˂ NTA Effector Cell Center ⎯⎯⎯⎯˂ NTA Ganglion⎯⎯⎯˂ NTA Effector Cell



Process of Exocytosis Calcium → Synaptotagmin → Ca-Synaptotagmin complex → becomes heavy (goes down) → Synaptobrevin →
Syntaxin, SNAP 25 → fuse in nerve terminal → exocytosis → bind in receptors → elicit response (physiological)

SOURCES:
• Dra. Valerio’s discussion and presentation




FAR EASTERN UNIVERSITY – NICANOR REYES MEDICAL FOUNDATION
Physiology A
Gloria Marie M. Valerio, MD
AUTONOMICS
1. Synthesis and Storage of neurotransmitter agent – synthesis in the ribosomes; stored in secretory vesicles 

2. Release of NTA at the synaptic cleft – motor impulse reaches nerve ending; highly permeable to Calcium ions
Steps in Biochemical (influx); interaction of membrane proteins - Syntaxin and synaptobrevin – cause vesicles to fuse with nerve terminal
Transmission membrane; exocytose the NTA into the synaptic cleft 

3. Interaction - NTA binds with receptors and elicits a physiologic response from effector cell 

4. Deactivation of NTA – unbinding from the receptor 

1. LIGAND GATED/ ION CHANNELS (IONOPHORE)
NTA + Receptor → Open Ion Channels
If Na+ channels, Na+ influx, depolarization will lead to excitation 

If K+ channels, K+ efflux, hyperpolarization will lead to inhibition 

If channels are on effector cell, elicit an 
immediate but short-lived response from the effector cell.

Ex. Ach + Nicotinic Receptors (Skeletal Muscle) → Ach + Nicotinic: Ligand gated channel
2. G PROTEIN COUPLED RECEPTORS
NTA + Receptor → activate G Protein → activate intracellular enzymes → secondary messengers
Ex.
☛Activate specific intracellular (I/C) enzymes 
that will lead to formation of intracellular ligands (aka Second
Messengers), which will mediate the action of the NTA on the effector cell. 

☛Produces a delayed response but longer duration that persists even if NTA is no longer present.


a. NTA + Receptor → activate G-Proteins → activate enzyme system, (+) Adenylyl cyclase → formation of ↑cAMP
(cyclic adenosyl monophosphate is the intracellular ligand or second messenger) → activate (+) protein kinase
A → phosphorylation of other enzymes that will elicit specific responses from the cell

Catecholamines (Nor, EP) + beta receptors
RECEPTORS Acetylcholine + muscarinic receptors
beta receptors and muscarinic receptors are G-protein coupled receptors


Summary:
NTA+R → (+) G Protein → (+) enzyme → adenylyl cyclase → ↑CAMP → (+) protein kinase → phosphorylate IC
enzymes → (+) biochemical rxn

b. NTA + Receptor activate G-Proteins activate enzyme system, (+) phospholipase C → breakdown of
phosphoinositol biphosphate PIP2, forming 2 products:
☛Inositol triphosphate IP3 → increase I/C Ca2+; Calcium can function as second messenger
☛Diacyl glycerol DAG → (+) Protein kinase C → causes phosphorylation of I/C proteins → stimulate specific
biochemical responses from the cell
Catecholamines + alpha receptors
Ach + muscarinic receptors (depending on location in the body)

Summary:
NTA+R → (+) G Protein → (+) Phospholipase C → Breakdown of PIP2 → ↑IP3 (I/C Ca++)
↓
DAG → (+) PKC → Phosphorylates I/C CHONS
ENZYMATIC DEACTIVATION
Ex. Ach deactivation by acetylcholinesterase
deactivation by enzymes in the synaptic cleft

1. Cholinergic effects short in duration
RE-UPTAKE
Ex. Deactivation of norepinephrine at neuro junction
Deactivation of NTA 1. After unbinding from the receptor 

2. Actively transported back in the terminal but 
will not be stored in vesicles. These will be destroyed by
monoamineoxidase (MAO)
3. Other NEP: circulated in the blood and transported to the liver, where NEP is deactivated by enzyme catechol-O-
methyl transferase (COMT) - DIFFUSION
DIFFUSION AWAY FROM SYNAPSE
Ex. Circulating NE & E
NE & E is degraded primarily by MAOI (reuptake), secondarily in the liver by COMT
Present in:
1. All somatic neuromuscular junction (Somatic to skeletal muscle) 

2. All autonomic ganglia (all preganglionic to all postganglionic in both SNS and PSNS) 

Cholinergic transmission 3. All parasympathetic Neuroeffector Junctions (all PS effects to internal organs; biochemically, PSNS –
Cholinergic division; PSNS division is CRANIOSACRAL (anatomically) & CHOLINERGIC (biochemically)) 

4. Sympathetic cholinergic Neuroeffector Junctions, only if effectors are sweat glands and vascular smooth

muscles present in skeletal muscles. 


SOURCES:
• Dra. Valerio’s discussion and presentation




FAR EASTERN UNIVERSITY – NICANOR REYES MEDICAL FOUNDATION
Physiology A
Gloria Marie M. Valerio, MD
AUTONOMICS

present in:
Adrenergic transmission 5. All sympathetic adrenergic Neuroeffector Junction (NEJ) (all sympathetic effects to internal organs)
SYMPATHETIC DIVISION is THORACOLUMBAR (anatomically) and NORADRENERGIC (biochemically).

Sympathetic Cholinergic Sympathetic Adrenergic

Somatic NS Parasympathetic NS
(Syncholinergic) NS (Synadrenergic) NS
** Only in sweat glands and vascular
** most sympathetic effects to internal organs
smooth muscles present in skeletal muscles
are mediated by NEP


C C C C
⏐ ⏐ ⏐
⏐
⅄ Ach (N) ⅄ Ach (N)
⏐ ⅄ Ach (N)
⏐ PG PG PG
⏐ ⏐ ⏐
⏐
⅄ Ach (N) ⅄ Ach (M) ⅄ Ach (M)
⅄ NE (α1 ,α2,β1, β2)
EC EC EC EC

TRANSMISSION MEDIATED BY ACETYLCHOLINE
1. Synthesis of Acetylcholine: Choline + Acetyl Coa → Ach, catalyzed by Choline Acetyl Transferase. It will be
stored temporarily in vesicles located at the nerve ending. 

2. (Release) When an AP reaches the nerve ending, there will be Ca2+ influx, which will cause Ach to be released
CHOLINERGIC TRANSMISSION into the synaptic cleft. 

3. (Interaction) Ach binds to membrane receptors (cholinergic receptor) on the effector cell. 

4. (Deactivation) Main mechanism is enzymatic destruction/deactivation by Acetylcholinesterase, which is also
present in the synaptic cleft, where it can immediately deactivate acetylcholine. This makes cholinergic or
Parasympathetic effects short in duration.

Nicotinic (IONOPHORES) Muscarinic (METABOPHORES)
can also be stimulated by small dose of nicotine can be stimulated by small doses of muscarine
☛Present in all somatic neuromuscular junction (N1) ☛all parasympathetic neuroeffector junction 

☛Present in all autonomic peripheral ganglia (N2) ☛all sympathetic cholinergic neuroeffector junction
(sweat glands, vascular smooth 

muscle present in the skeletal muscle)

Mainly made of proteins. ☛Subdivided into M1-M5: 

classified as Ligand-gated receptor: M1 – brain, stomach (if M1 receptors in stomach is
(+) open Na+ channel 
 stimulated, increase in gastric secretion)

CHOLINERGIC RECEPTORS
Always elicits an excitatory reaction 
 M2 – most abundant heart and visceral smooth
muscles
M3 – visceral smooth muscles and glands

M4 – visceral smooth muscles and glands
M5 – least abundant; present only in sphincter
muscles of the iris, esophagus, parotid glands, cerebral
blood vessels
☛G-protein coupled receptor response may be either
excitatory or inhibitory.
TRANSMISSION MEDIATED BY NEP
1. Synthesis of NEP:
a. Steps:

phenylalanine → β tyrosine, catalyzed by phenylalanine hydroxylase.
β tyrosine → DOPA, catalyzed by tyrosine hydroxylase.

DOPA → Dopamine, catalyzed by DOPA decarboxylase.

Dopamine → Norepinephrine, catalyzed by dopamine β-hydroxylase. 

b. Location: at the nerve ending of sympathetic adrenergic efferent / postganglionic nerve endings. 

ADRENERGIC TRANSMISSION c. Regulation: by a negative feedback mechanism; if there is an excess of dopamine and 
norepinephrine,
it will cause inhibition of the enzyme Tyrosine Hydroxylase. 

d. A sagittal section of adrenal glands reveals 2 parts: 

outer part: adrenal cortex (secretes steroid hormones)

inner part: adrenal medulla (converts norepinephrine → epinephrine
• catalyzed by phenylethanolamine-N-methyl transferase)
e. Sympathetic adrenergic postganglionic nerve endings can synthesize/release NEP only.
Adrenal
medulla can synthesize/release both NEP and EP (collectively known as catecholamines). 


SOURCES:
• Dra. Valerio’s discussion and presentation




FAR EASTERN UNIVERSITY – NICANOR REYES MEDICAL FOUNDATION
Physiology A
Gloria Marie M. Valerio, MD
AUTONOMICS
2. (Release) When an AP reaches the nerve ending, there will be Ca2+ influx, which will cause NEP to be released
into the synaptic cleft. 

3. (Interaction) NEP or EP binds to membrane receptors (noradrenergic or adrenergic receptors) on the effector
cell. 

4. (Deactivation) Main mechanism is reuptake. Actively transported back in the terminal but will not be stored in
vesicles. These will be destroyed by Monoamine Oxidase (MAO). Other NEP: circulated in the blood and
transported to the liver, where NEP is deactivated by enzyme catechol-O-methyl transferase (COMT). This makes
adrenergic or Parasympathetic effects short in duration. 

α1
 β1

☛Present in visceral smooth muscles and glands ☛Only in heart
α2 β2

☛Present only at nerve terminal 
 ☛Present in visceral smooth muscles and glands
☛NEP+ α2 NEP inhibition 

☛Negative feedback mechanism Beta receptors when stimulated, elicit mostly
☛inhibit further release of norepinephrine 
inhibitory reaction (exemptions below)

Alpha receptors when stimulated, mostly elicit Examples:
excitatory reaction (exemptions below) ☛NEP + smooth muscle receptors in Bronchial wall,
ADRENERGIC RECEPTORS
smooth muscles relax = bronchodilation 

Examples: ☛EP+ β2 Vascular smooth muscle, muscle relaxes =
☛NEP+ α1 Radial muscle of iris, muscle 
contracts vasodilation 

(excitatory) = increase in 
pupillary size
☛EP+ α1 vascular smooth muscle, muscle 
contracts Exemptions: heart, bronchial glands, pancreatic
(excitatory) = vasoconstriction islets, effects are excitatory 


Exemptions: Digestive system, pancreatic islets,
bronchial gland, effects are inhibitory 


Cholinergic Adrenergic
M1 Brain, Stomach α1 Visceral Smooth Muscles, Glands
M2 Heart α2 Nerve Terminals
M3 Visceral Smooth Muscles β1 Heart
M4 Visceral Smooth Muscles, Locomotion β2 Visceral Smooth Muscles, Glands

M5 Sphincter of iris, Esophagus, Parotid gland, Cerebral BV β3 Adipose

Sympathetic preganglionic fibers
↓Ach
(N) Adrenal Medulla
↓
NEP (80%) +EP (20%)
SYMPATHETIC PREGANGLIONIC FIBERS ↓
Circulation NOT in NEJ (therefore indirect effect)
↓
(+) α1, β1, β2 receptors
↓
↑sympathetic adrenergic effects
NOREPINEPHRINE Strongly stimulates α receptors and only weakly stimulates β1, β2 receptors

EPINEPHRINE Strongly stimulates α, β1, β2 receptors

Sympathetic NS and PSNS are PHYSIOLOGIC ANTAGONISTS, produces opposite effects.
1. DUAL innervation of the SAME STRUCTURE of the SAME ORGAN produces OPPOSITE EFFECTS.
Ex. Heart 
Sympathetic N (↑HR) SA Node ß Vagus/CNX, Parasympathetic (↓HR) 

2. DUAL innervation of 2 DIFFERENT STRUCTURES in the SAME ORGAN produces OPPOSITE EFFECTS.
Ex. Eyeball – Pupil regulates the amount of light entering the eye

Iris: radial muscle (Sympathetic): absence of light pupil dilates

AUTONOMIC INNERVATION
Sphincter muscle (Oculomotor CN3 parasympathetic): presence of light pupil constricts 

3. DUAL innervation of 2 DIFFERENT STRUCTURES in the SAME ORGAN produces SYNERGISTIC EFFECTS. Ex.
Salivary gland 
Para: profuse increase in salivary secretion: loose, watery secretion Sympa: mild moderate
increase in salivary secretion: viscous secretion 

4. SINGLE innervations
NO PARASYMPATHETIC INNERVATION. SYMPATHETIC INNERVATION ONLY.
Ex.
Kidneys, sweat gland, pilo arrector muscle in skin, vascular smooth muscle 


SOURCES:
• Dra. Valerio’s discussion and presentation




FAR EASTERN UNIVERSITY – NICANOR REYES MEDICAL FOUNDATION
Physiology A
Gloria Marie M. Valerio, MD
AUTONOMICS

PHYSIOLOGICAL DIFFERENCES
Difference Sympathetic Nervous System (SNS) Parasympathetic Nervous System (PSNS)
Energy CATAbolic ANAbolic
Longer, Prolonged duration
Reason: Norepinephrine at NEJ that is not immediately Short duration
Duration deactivated; additionally mediated by norepinephrine Reason: Mediated by Ach, immediately deactivated
and epinephrine in the blood stream

Fight or Flight
Rest and Digest
Effects Stimulation of sympathetic nerves enables individuals to
Conservation/ restoration of the body’s processes
cope or withstand stressful conditions
Generalized diffuse response
Localized response except Vagus nerve
Response Reason: extensive branching of the pre- ganglionic
Reason: limited branching, except for Vagus nerve
fibers
Coordinated; but some processes do not have to
Timing Coordinated; response occurs at the same time occur at the same time
(ex. micturation, defecation, erection)
Head ganglion of the ANS – Hypothalamus
Anterior hypothalamus – coordinates 
Cholinergic
activities

Center
Posterior/ Lateral hypothalamus – 
coordinates
Adrenergic activities 


PHARMACOLOGIC DIFFERENCES
Sympathetic Nervous System (SNS) Parasympathetic Nervous System (PSNS)
ADRENERGIC CHOLINERGIC
Cholinergic
↑ / Potentiate cholinergic or parasympathetic effect

Adrenergic
↑ / Potentiate adrenergic or sympathetic effect
↑ synthesis of Ach

↑ synthesis of NEP

↑ release of Ach

↑ release of NEP

↑ interaction between Ach and cholinergic receptor

↑ interaction between NEP and adrenergic receptor

(-) deactivation of Ach
(-) inactivation of NEP

PARASYMPATHOMIMETIC – mimics the effects of parasympathetic
SYMPATHOMIMETIC –mimics the effects of sympathetic stimulation
stimulation
ANTIADRENERGIC ANTICHOLINERGIC
↓ / Block adrenergic or sympathetic effect synthesis of NEP
 ↓ / Block cholinergic or parasympathetic effect synthesis of Ach

↓ release of NEP Block interaction between NEP & adrenergic receptor
 ↓ release of Ach
Block interaction bet. Ach & cholinergic receptor

↑ deactivation of NEP SYMPATHOLYTIC ↑ inactivation of Ach
PARASYMPATHOLYTIC

SOURCES:
• Dra. Valerio’s discussion and presentation