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PHARMACOLOGY - 2 > 14 –Autonomic Nervous System > Flashcards

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
Q

Those with disease or lots of oxidated stress: endothelium damage

A
  • 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
Q

Viagar (sildenafil)

A
  • 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
Q

Cholinergic neurotransmission:

A
  • 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
Q

Botulinum toxin

A
  • 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
Q

Cholinesterase inhibitors

A
  • 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
Q

Acronym to remember effects of cholinesterase inhibitors (high levels of ACh): SLUD

A
  • Salivation
  • Lacrimation
  • Urination
  • Defecation
  • *also no blood flow
31
Q

Black widow spider venom

A
  • 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
Q

Adrenergic neurotransmission:

A
  • Tyrosine to dopa to dopamine into vesicles then inside converted to NE
  • Off signal=reuptake by presynaptic nerve
33
Q

Metyrosine

A
  • 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
Q

Amphetamine

A
  • 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
Q

Cocaine

A
  • 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
Q

Monoamine oxidase (MAO) inhibitors

A
  • 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
Q

Bretylium

A
  • Prevents NE release
  • ANTI-ADRENERGIC EFFECT
38
Q

ACh-esterase inhibitors: irreversible vs. reversible

A
  • Irreversible: insecticides (toxic)
    o If haven’t died: can give anti-muscarinic drugs
  • Reversible: edrophonium
39
Q

Nicotinic receptors (Nm) on muscle

A
  • Opening of Na channel=depolarization=AP to cause muscle contraction
  • Off signal=ACh-esterase
40
Q

Antagonists of Nm receptors

A
  • Pancuronium
  • *can use to Ach-esterase inhibitors to ‘outcompete’ them
  • Succinylcholine
41
Q

Pancuronium

A
  • competitive antagonist for ACh at Nm receptors
  • *used when need flaccid paralysis
    o Do NOT want it to paralyze the diaphragm though
42
Q

Succinylcholine

A
  • 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)

PHARMACOLOGY - 2 (16 decks)

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