19. ANS Pt 2

Question 1

What are the targets of PNS?

Answer 1

1. Smooth muscle (gut, resp. syst, vasculature)
2. Cardiac muscle
3. Glands (hormones, digestive enzmes, tears)

Question 2

What are PNS effects?

Answer 2

• PNS brings body to most efficient state

1. Salivation
2. Lacrimation
3. Urination
4. Digestion (metabolism, peristalsis, breakdown + uptake of nutrients)
5. Defecation
6. Pupillary constriction
7. Vasomotor control (balanced by SNS output: BP, blood flow)
8. Bronchial control (balanced by SNS: bronchial dilation for bigger breaths)

• SNS wastes E + takes away from organ reserve

Question 3

What is the major parasympathetic nerve?

Answer 3

• Vagus = “wandering”
• Comes out of brainstem + Innervates thoracic + abd structures (SNS ganglia tend to be more organ sp.)
• 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

Question 4

What are PNS NT + receptors called?

Answer 4

• NT = Ach
  
  • B/c ACh = NT for neuromuscular jxn, anything that impacts PNS will also affect motor end plates
• Receptor = cholinergic receptor

Question 5

How is ACh synthesized?

Answer 5

• Synthesized in cholinergic neurons
• Acetyl Co-A + choline –(choline acetyltransferase)–> ACh

Question 6

Where are ACh stored?

Answer 6

ACh stored in vesicles at nerve end terminals (both pre + post-ganglionic nerve terminals)

Question 7

What 2 types of receptors are found on distal organs interfacing w 2nd nerve?

Answer 7

1. Muscarinic receptors
2. Nicotinic receptors

Question 8

ACh re-uptake is facilicated by _____ coupled to Na-K-ATPase pump.

Answer 8

High affinity Na-choline co-transport

Question 9

How is ACh released?

Answer 9

1. Depolarization of nerve terminal –> influx of Ca++
2. Ca++ stimulates + promotes vesicular exocytosis of NT into cleft

Question 10

What is 1 example of a toxin that prevents acetylcholine release? What happens as result?

Answer 10

• Botulinum Toxin A
• Binds to vesicles + prevents exocytosis (–> no neuromuscular jxn fxn)
• Leads to flaccid paralysis + resp. failure

Question 11

How is ACh activity terminated?

Answer 11

1. Reuptake –> can be reused
2. 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

Question 12

What is 1 parasymathetic consequence of using muscle relaxant reversals?

Answer 12

Increase in ACh affects both neuromuscular jxn + PNS –> huge parasympathetic output (=reason we give glyco)

Question 13

What are 4 cholinesterase inhibitors?

Answer 13

1. Neostigmine
2. Edrophonium
3. Pyridostigmine
4. Physostigmine

Increased ACh leads to increased ACh diffusing away from synapse into bloodstream –> more distal + PNS effects

Question 14

What kind of receptors are nicotinic receptors?

Answer 14

• Nicotinic receptors = ligand-gated ion channels
  
  • Ligand: nicotine or ACh
  • ACh binds ⍺-subunits
• Location: neuromuscular jxn + autonomic ganglia (PNS + SNS)

Question 15

What happens when nicotinic receptors are activated?

Answer 15

1. Stimulation (ACh binds ⍺-subunits)
2. Nicotinic receptor ion channel opens
3. Na + K flow down concentration gradient –> depol
4. Further stim of another nerve or other outcome (secretion, smooth muscle contraction…)

Question 16

What kind of receptors are muscarinic receptors?

Answer 16

• 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)

Question 17

What happens when muscarinic receptors are activated?

Answer 17

1. Stimulation
2. G-protein activation
3. Pospholipase C activation: phosphatidylinositol 4,5-bisphosphate –> IP3 + DAG
4. IP3 –> increased Ca++ from SR
5. Smooth muscle contraction + glandular secretion

Question 18

(T/F) Binding of ACh to muscarinic receptor leads to vasoconstriction.

Answer 18

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

Question 19

(T/F) ACh induced NO release by endothelial cells can cause systemic vasodilation.

Answer 19

False.

NO can’t cause systemic vasodilation b/c breaks down quickly –> would breakdown as diffusing away

Question 20

Does release of Ca++ by ACh binding to muscarinic receptor increase contraction + conduction?

Answer 20

No. Slows conduction + decrease HR!

M2 receptors mediate inhibition via G-proteins –> hyperpolarization + slower spontaneous depol

Question 21

What is a cholinergic crisis?

Answer 21

• Upregulated + uncontrolled increase in PNS
• Causes:
  
  1. Mydriasis (crying)
  2. Miosis (pupillary dilation)
  3. Perspiration
  4. Salivation
  5. Bronchoconstriction
  6. Broncial secretions –> bronchospasm + laryngospasm
  7. Flaccid paralysis
  8. Respiratory failure
• Treatment: anticholinergic drugs to block side effects

Question 22

Summary of cholinergic receptor action.

Answer 22