Autonomic Nervous System Flashcards
2 divisions of the ANS
sympathetic
parasympathetic
Both systems are (3)
Involuntary, Excitatory & Inhibitory, Di-synaptic
Generally — one another when they innervate the same tissue.
oppose
Each system is — active, but one system is usually
predominant at rest.
tonically
Sympathetic (SNS) (3)
• Fight or Flight • Can selectively activate effectors or elicit a mass discharge, especially during stress response • Noraderenergic (NE)/Adrenergic (EPI) – BUT cholinergic pre- to post-ganglionic
Parasympathetic (PNS) (3)
• Rest & Digest • Control mechanisms are almost always specific, activating or inhibiting discrete targets. • Cholinergic (ACH)
Both the SNS & PNS have: (2)
Preganglionic neurons
Postganglionic neurons
Preganglionic neurons (cell bodies in
lateral gray horn of the
spinal cord (SNS) or motor nuclei
of cranial nerves III, VII, IX and X
(PNS))
All preganglionic terminals
release
ACh that binds to
nicotinic receptors (Type NN)
on the postganglionic neuron
— receptors are ligand-
gated ion channels (ionotropic)
that are selective for both (2)
nACh
Na+
and K+.
Postganglionic neurons cell
bodies are
outside of the CNS
Thoracolumbar Division
T1 through L3 or L4
Preganglionic axons exit through a white ramus into one of
the ganglia of the sympathetic chain. Fibers will then either: (4)
1. Synapse with postganglionic neurons at that ganglia 2. Pass up or down the sympathetic chain, then synapse with a different ganglia 3. Pass through the chain and out a sympathetic nerve (Splanchnic) where it will synapse in a peripheral sympathetic ganglion (celiac, superior mesenteric, or inferior mesenteric) 4. EXCEPTION: Adrenal Medulla
Almost all sympathetic postganglionic terminals release
— which —
norepinephrine (NE/noradrenaline) at synapse with target cells.
NE activates both alpha and beta receptors.
Almost all sympathetic postganglionic terminals release
norepinephrine (NE/noradrenaline) at synapse with target cells.
NE activates both alpha and beta receptors.
– Exception:
most sympathetic post-ganglionic terminals release ACh
at sweat glands to activate muscarinic receptors. Some skeletal
muscle vasculature also works this way.
When stimulated, the adrenal medulla (chromaffin cells)
secretes
80% epinephrine (EPI/adrenaline) and 20% NE into
the bloodstream. EPI and NE then circulate throughout the
body and activate adrenergic receptors.
The adrenal medulla contains the enzyme —, which catalyzes the conversion of NE to
EPI (this reaction requires cortisol)
phenylethanolamine-N-
methyltransferase (PNMT)
Compared to beta receptors, alpha receptors have a –
affinity for catecholamines, so beta receptors are activated at
lower lower concentrations (i.e. beta receptors have a higher affinity)
Norepinephrine has a slightly greater potency at —
receptors compared to epinephrine.
alpha
Alpha 1:
constrict smooth muscle (Gq protein, increase IP3)
Alpha 2:
blocks further NE release (presynaptic receptor) (Gi
protein, decrease cAMP)
Catecholamine Potency for Beta receptors varies: (3)
Epi & NE have almost equal potency at beta 1 receptors;
Epi has MUCH greater potency at beta 2 receptors than NE;
NE has slightly greater potency at beta 3 receptors than EPI.
Beta 1:
increase heart rate & contractility, increase lipolysis, increase
renin secretion, increase protein content in saliva (Gs
protein: increase cAMP)
Beta 2:
relax smooth muscle, release FA & glucose (Gs protein: increase
cAMP)
Beta 3:
found in adipose tissue (Gs protein: increase cAMP)
Systemic absorption of injected local anesthetics depends on
blood flow to the area.
The addition of epinephrine causes
vasoconstriction (via alpha 1 receptors) at the site of administration, which decreases blood absorption and facilitates neuronal uptake, enhances quality of analgesia, prolongs duration of action and limits toxic side effects. Addition of EPI to lidocaine usually extends the duration of anesthesia by at least 50%.
Albuterol
Beta 2 selective agonist, is used for treatment of asthma
as it causes bronchodilation.
NE that is released by nerve terminals
remains active for only a few seconds
before: (3)
- Diffusion away from synaptic cleft
- Reuptake by presynaptic terminal
(cocaine blocks re-uptake) - Destruction by the enzymes
MonoAmine Oxidase (MAO) or
Catechol-O-Methyl Transferase (COMT)
PNS compared to SNS: (2)
– PNS has longer preganglionic axons than SNS. – Preganglionic terminals also release ACh that binds to nicotinic ACh receptors.
Craniosacral Division (2)
– Preganglionic parasympathetic axons supply the face via the oculomotor (III), facial (VII), glossopharyngeal (IX) nerves and the thorax and upper abdomen via the vagus (X) nerve. – S2-4 carry preganglionic parasympathetic axons to the pelvic viscera.
Postganglionic parasympathetic varicosities release
ACh that bind
to muscarinic ACh receptors on target cells.
Muscarinic receptors (G-protein/metabotropic) (3)
– Constrict smooth muscle
– Relax sphincters
– Stimulate glandular secretions
Known Muscarinic Receptors (4)
– M1
– M2
– M3
– M4
– M1:
stomach (secretions and contraction), salivary glands (Gq: IP3, increase IC Ca++)
– M2:
smooth muscle, myocardium, cardiac autorhythmic cells, CNS (Gi protein, decrease cAMP)
– M3:
exocrine glands (ex. salivary), smooth muscle, endothelium, CNS (Gq: IP3, increase IC Ca++)
– M4:
CNS, vagal nerve (Gi protein, decrease cAMP)
Cholinergic Receptors (5)
– M1 – M2 – M3 – M4 _ M5
M5:
sweat glands (SYMPATHETIC FUNCTION) (Gq: IP3, increase IC Ca++)
Anticholinergic drugs such as amitriptyline (Elavil), a
tricyclic antidepressant, inhibit the effects of
acetylcholine systemically (via muscarinic receptors), resulting in a myriad of side effects. Gastrointestinal side effects include xerostomia, constipation, ileus, and nausea and vomiting.
• Sialorrhea (drooling) can occur in patients taking
anti-cholinesterases (ex. treatment for Alzheimer’s Disease).
Skeletal Muscle: Binding of ACh to NM receptor elicits
contraction
Relaxation occurs when
ACh release by the somatic motor neuron and activation of NM receptor stops
PNS: bladder (2)
M2 Relax sphincter
M3 Constricts detrusor
SNS: bladder (2)
alpha1 Constricts sphincter
beta2 Relaxes detrusor
PNS: GI Tract (2)
M2 Relax sphincter
M3 Contracts muscle
SNS: GI Tract (2)
alpha1 Constricts sphincter
beta2 Relaxes muscle
PNS :Salivary Glands
M1 and M3 Stimulates lots of watery secretion due to contraction of myoepithelial cells and vasodilation
SNS: Salivary Glands (2)
alpha1 vasoconstriction and secretion of concentrated saliva
beta1 receptors stimulate secretion of protein
anti-cholinergic drugs for the treatment of Parkinson’s Disease can cause
Xerostomia
Methamphetamine acts on the α -adrenergic receptors of the vasculature of the salivary glands, causing vasoconstriction and reducing salivary flow, depriving the oral environment of saliva's buffering activity to counteract acidity and prevent demineralization of enamel leading to
“Meth Mouth”.
PNS: vascular smooth muscle/blood
NA
SNS: vascular smooth muscle/blood
alpha1 vasoconstriction
beta2 vasodilation
the diameter of most arterioles in the body is not regulated by the PNS, but there are a few exceptions. For example, the PNS (via ACH on Muscarinic Receptors) causes
vasodilation of salivary gland arterioles,
which increases blood flow to the salivary glands for secretion of saliva. A few other arterioles that dilate
under PNS control include arterioles of the gastric and intestinal glands.
PNS: Heart
Keeps HR low (M2)
SNS: heart
increases HR and contractility (beta 1) and coronary blood flow via vasodilation (beta 2)
PNS: lungs
predominant tone
constricts bronchial smooth muscle (M3)
SNS: lungs
relaxes bronchial smooth muscle (beta2)
