14 –Autonomic Nervous System Flashcards

1
Q

NTs: somatic nerves

A
  • ACh: nicotinic receptor
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2
Q

Receptors in ganglia are always

A
  • Nicotinic
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3
Q

NTs: preganglionic nerve onto adrenal medulla

A
  • ACh: nicotinic receptor
    o E+NE released into blood
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4
Q

NTs: pre-ganglionic sympathetic nerves

A
  • ACh: nicotinic
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5
Q

NTs: post-ganglionic sympathetic nerves

A
  • NE
    o Heart: beta-1
    o Smooth muscle : alpha-1,
     E from the blood: beta-2
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6
Q

NTs: pre-ganglionic parasympathetic nerves

A
  • ACh: nicotinic
    o Exocrine glands: M3
    o Heart: M2
    o Smooth muscle : M3
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7
Q

NTs: post-ganglionic PS nerves

A
  • ACh
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8
Q

Sympathetic NS: ‘spinal segments’

A
  • Preganglionic nerves exit spin in thoracic and lumbar nerves
  • Sympathetic chain ganglion: synapses above and below
    o *Responses tend to be ALL OR NONE!
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9
Q

Parasympathetic NS: ‘spinal segments’

A
  • Cranial and sacral nerves
  • Longer pre-ganglionic neuron
  • Ganglion may be in the ‘target organ/tissue’
  • Discrete activation
    o Can get one nerve activated without activated another
  • *vagus is major player
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10
Q

Baroreceptor reflex

A
  1. Increased arterial pressure=stretch of baroreceptors in aortic arch and carotid artery
  2. Vasomotor center:
    a. Decreased sympathetic impulses on arterioles=vasodilation
    b. Increase PS impulses mainly on heart=decrease HR= decrease CO=decrease BP
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11
Q

Agonist is

A
  • Substance that binds to a receptor and activates it
  • Can be an exogenous chemical (drug)
  • Mimics actions of an endogenous ligand
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12
Q

Antagonist is

A
  • Substance that binds to a receptor, but prevents its activation
  • Blocks effects of drugs that activate the receptor
  • Blocks effects of endogenous activators of a receptor
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13
Q

PS vs S

A
  • Effects generally oppose each other (physiological systems that antagonise each other)
  • One system will have predominant ‘tone’ over the other in a given organ
    o Resting: PS should be predominant (exception: arterioles)
  • Blocking one system often UNMASK activity of opposing system
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14
Q

Arterioles

A
  • Main controller of BP
  • Have no PS innervation!
  • Control BP through S innervation degree of activity
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15
Q

ACh cholinergic receptors: 2 major subtypes

A
  • Muscarinic: M1-M5
  • Nicotinic: Nm (skeletal muscle), Nn (neurons: ganglia or adrenal medulla)
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16
Q

Muscarinic receptors and drugs

A
  • Don’t have any drugs that aren’t toxic
  • *’dirty’: hit everything
    o Usually many side effects
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17
Q

NE and E adrenergic receptors: 2 major subtypes

A
  • Alpha-adrenergic: a1, a2
  • Beta-adrenergic: b1, b2, b3
18
Q

Beta-3

A
  • On many cells
    o adipocyte cells! (obesity)
  • Drugs for anti-obesity?
19
Q

Effects of IV infusion of NE at low to moderate dose

A
  • Increase in pulse pressure
  • Marked increase in peripheral resistance
  • Increase in systolic BP
  • increase in diastolic BP
  • *no increase in pulse rate as baroreceptor response
20
Q

Beta-1 adrenergic antagonist in a resting animal:

A
  • Decrease HR
  • Decrease force of contraction in heart
  • *vagal stimulation pre-dominates
21
Q

Beta-1 adrenergic antagonist in an agitated animal

A
  • Have significant sympathetic stimulation
    o *beta-blocker will slow HR and reduce contractility
22
Q

ANS receptor signal transduction

A
  • Beta-receptor (M3) activates Gs which stimulates adenyl cyclase=more cAMP=more PKA=effect
  • Alpha 2 and M2 receptors (heart)=activate Gi which inhibits adenylyl cyclase=less cAMP=decrease PKA=decreased biological effect
23
Q

How do you turn cAMP ‘off’?

A
  • Phosphodiesterase to get AMP
  • *if inhibit phosphodiesterase=get more cAMP=more biological effect
  • *same with cGMP
24
Q

Vascular endothelium and NO

A
  • M3-receptor on endothelium stimulated=activate IP3, DAG=Ca2+ and Ca-calmodulin and get NO
    o Short lived
    o Some into lumen of artery
    o LOTS diffuses into vascular smooth muscle cell
  • Muscle cell: stimulates guanyly cyclase=get cGMP=relaxation!
  • *Viagra prefers to work on this phosphodiesterase=get more dilation
25
Those with disease or lots of oxidated stress: endothelium damage
- Endometrium have decreased endothelial cells o Have M3 receptors on the smooth muscle cells as well (normally don’t see the effect)=activates Gq and get Ca2+ release=contraction - *does not matter for phosphodiesterase (separate, not dependent on NO): can still work when there is endothelial damage
26
Viagar (sildenafil)
- Phosphodiesterase inhibitor - Inhibits degradation of cGMP=greater effect in arteries - *vasodilate pulmonary arteries in pulmonary hypertension - No direct effects on cardiac system - Would slow progression of labour
27
Cholinergic neurotransmission:
- Acetate and choline = ACh - Uptake of ACh into presynaptic terminal vesicles - Released into synapse and bind N or M receptors - Continues to activate until acetylcholinesterase breaks it down to choline+acetate (OFF SIGNAL)
28
Botulinum toxin
- Blocks exocytosis (release) of ACh - ANTICHOLINERGIC EFFECT - *do NOT want to give systemically as it will stop all nerve function (including the diaphragm!) - Ex. humans; use for excessive sweating
29
Cholinesterase inhibitors
- Used to keep the ACh signalling ON - MASSIVE overflow and activation of N and M receptors - PROCHOLINERGIC EFFECT - Ex. insecticides (irreversible inhibitors of acetylcholinesterase) - Also have reversible=more controllable (to help with muscle function)
30
Acronym to remember effects of cholinesterase inhibitors (high levels of ACh): SLUD
- Salivation - Lacrimation - Urination - Defecation - *also no blood flow
31
Black widow spider venom
- Causes ACh release due to leakiness of cholinergic vesicles - PROCHOLINERGIC toxin o Milder version of SLUD and muscle twitching + activation compared to acetylcholinesterase inhibitors - *probably more than one spider needed to bit it (or it dies from anaphylaxis)
32
Adrenergic neurotransmission:
- Tyrosine to dopa to dopamine into vesicles then inside converted to NE - Off signal=reuptake by presynaptic nerve
33
Metyrosine
- Methylated tyrosine which then forms methyl-NE which will go in the vesicles and be released - *little to NO ability to activate alpha and beta receptors in tissue - ANTI-ADRENERGIC EFFECT o No enough NE to maintain normal tone in blood vessels=get vasodilation and drop in peripheral resistance=drop in BP - *old school: hypotension drug (almost TOO strong)
34
Amphetamine
- Causes NE to leak out of vesicles to release NE into nerve terminals - PRO-ADRENERGIC EFFECT - Causing activation of alpha and beta receptors (but in an indirect way)
35
Cocaine
- Blocks NE reuptake - More accumulation of NE than amphetamine - *also effects dopamine reuptake in dopaminergic cells - *mix of effects that give distinct effects=activate fight or flight
36
Monoamine oxidase (MAO) inhibitors
- Old anti-depressants in humans, but used in vet med INHIBIT it - Promotes more serotonin! (elsewhere) - Minor role: slightly more NE - Too many side effects in humans
37
Bretylium
- Prevents NE release - ANTI-ADRENERGIC EFFECT
38
ACh-esterase inhibitors: irreversible vs. reversible
- Irreversible: insecticides (toxic) o If haven’t died: can give anti-muscarinic drugs - Reversible: edrophonium
39
Nicotinic receptors (Nm) on muscle
- Opening of Na channel=depolarization=AP to cause muscle contraction - Off signal=ACh-esterase
40
Antagonists of Nm receptors
- Pancuronium - *can use to Ach-esterase inhibitors to ‘outcompete’ them - Succinylcholine
41
Pancuronium
- competitive antagonist for ACh at Nm receptors - *used when need flaccid paralysis o Do NOT want it to paralyze the diaphragm though
42
Succinylcholine
- Initially activates Na channels, but then stays on the Nm receptor=PARALYSIS - Twitching than paralysis - *common to use when intubating an animal (ex. relax trachea)