19. ANS Pt 2 Flashcards
What are the targets of PNS?
- Smooth muscle (gut, resp. syst, vasculature)
- Cardiac muscle
- Glands (hormones, digestive enzmes, tears)
What are PNS effects?
- PNS brings body to most efficient state
- Salivation
- Lacrimation
- Urination
- Digestion (metabolism, peristalsis, breakdown + uptake of nutrients)
- Defecation
- Pupillary constriction
- Vasomotor control (balanced by SNS output: BP, blood flow)
- Bronchial control (balanced by SNS: bronchial dilation for bigger breaths)
- SNS wastes E + takes away from organ reserve
What is the major parasympathetic nerve?
- Vagus = “wandering”
- Comes out of brainstem + Innervates thoracic + abd structures (SNS ganglia tend to be more organ sp.)
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Recurrent laryngeal nerve supplies motor innervation to all nerves of larynx except cricothyroid (–> superior laryngeal)
- Damage –> closing of vocal cords (nerve keeps cords open)
- Neck surgery, tumors, trauma involving carotid sheath (carotid artery, jugular vein + vagal nerve) –> hoarse voice
- Bilateral damage results in midline position of vocal cords, stridor, laryngeal obstruction
What are PNS NT + receptors called?
- NT = Ach
- B/c ACh = NT for neuromuscular jxn, anything that impacts PNS will also affect motor end plates
- Receptor = cholinergic receptor
How is ACh synthesized?
- Synthesized in cholinergic neurons
- Acetyl Co-A + choline –(choline acetyltransferase)–> ACh
Where are ACh stored?
ACh stored in vesicles at nerve end terminals (both pre + post-ganglionic nerve terminals)
What 2 types of receptors are found on distal organs interfacing w 2nd nerve?
- Muscarinic receptors
- Nicotinic receptors
ACh re-uptake is facilicated by _____ coupled to Na-K-ATPase pump.
High affinity Na-choline co-transport
How is ACh released?
- Depolarization of nerve terminal –> influx of Ca++
- Ca++ stimulates + promotes vesicular exocytosis of NT into cleft
What is 1 example of a toxin that prevents acetylcholine release? What happens as result?
- Botulinum Toxin A
- Binds to vesicles + prevents exocytosis (–> no neuromuscular jxn fxn)
- Leads to flaccid paralysis + resp. failure
How is ACh activity terminated?
- Reuptake –> can be reused
- Hydrolysis to acetate + choline –> can be reused
- Accel. by acetylcholinesterase prim. in synapse
- Butyrylcholinesterase (pseudocholinesterase) –> circulating hydrolysis in bloodstream
- Diffusion away is minimal due to high enzyme activity
What is 1 parasymathetic consequence of using muscle relaxant reversals?
Increase in ACh affects both neuromuscular jxn + PNS –> huge parasympathetic output (=reason we give glyco)
What are 4 cholinesterase inhibitors?
- Neostigmine
- Edrophonium
- Pyridostigmine
- Physostigmine
Increased ACh leads to increased ACh diffusing away from synapse into bloodstream –> more distal + PNS effects
What kind of receptors are nicotinic receptors?
- Nicotinic receptors = ligand-gated ion channels
- Ligand: nicotine or ACh
- ACh binds ⍺-subunits
- Location: neuromuscular jxn + autonomic ganglia (PNS + SNS)
What happens when nicotinic receptors are activated?
- Stimulation (ACh binds ⍺-subunits)
- Nicotinic receptor ion channel opens
- Na + K flow down concentration gradient –> depol
- Further stim of another nerve or other outcome (secretion, smooth muscle contraction…)
What kind of receptors are muscarinic receptors?
- At least 5 types:
- M1 - autonomic ganglia + CNS
- M2 - supraventricular cardiac (brady + negative inotropic effect)
- M3 - smooth muscle + glands (depending on location –> constraction or dilation of smooth muscles + release of secretions from glands)
What happens when muscarinic receptors are activated?
- Stimulation
- G-protein activation
- Pospholipase C activation: phosphatidylinositol 4,5-bisphosphate –> IP3 + DAG
- IP3 –> increased Ca++ from SR
- Smooth muscle contraction + glandular secretion
(T/F) Binding of ACh to muscarinic receptor leads to vasoconstriction.
False.
ACh stim. production of NO by endoendothelial cells –> vasodilation. Without endothelial cells, ACh leads to smooth muscle contraction
- NO = very potent but shortlived vasodilator, works on smooth muscle cells
(T/F) ACh induced NO release by endothelial cells can cause systemic vasodilation.
False.
NO can’t cause systemic vasodilation b/c breaks down quickly –> would breakdown as diffusing away
Does release of Ca++ by ACh binding to muscarinic receptor increase contraction + conduction?
No. Slows conduction + decrease HR!
M2 receptors mediate inhibition via G-proteins –> hyperpolarization + slower spontaneous depol
What is a cholinergic crisis?
- Upregulated + uncontrolled increase in PNS
- Causes:
- Mydriasis (crying)
- Miosis (pupillary dilation)
- Perspiration
- Salivation
- Bronchoconstriction
- Broncial secretions –> bronchospasm + laryngospasm
- Flaccid paralysis
- Respiratory failure
- Treatment: anticholinergic drugs to block side effects
Summary of cholinergic receptor action.
