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NS_BTRAN > Autonomic Nervous System Neuropharmacology > Flashcards

Autonomic Nervous System Neuropharmacology Flashcards

1
Q

What are the mechanism by which ANS drugs act? (3)

A
  • Direct Agonist
  • Antagonist
  • Indirect Agonist/Antagonist
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2
Q

ANS drugs that act to mimick NT action at receptor level are ?

A

Direct Agonist

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3
Q

ANS drugs that act to block NT action at receptor level are ?

A

Antagonist

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4
Q

What is the MOA of Indirect Agonist/Antagonist ANS drugs?

A

Change normal action of NT.

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5
Q

Indirect Agonist/Antagonist ANS drugs change normal action of NT, in what ways do they/can they do this?

A
  • Synthesis of NT.
  • Storage and release of NT.
  • Inactivation of NT following release. (*Less clinically useful because they affect all synapses for that particular NT regardless of which specific postsynaptic receptor subtype is present.)
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6
Q

Most clinically useful are drugs that act at the ____ (post or pre?) -synaptically at specific receptor subtypes as agonists or antagonists

A

POST!

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7
Q

Between a direct agonist and a direct antagonist ANS drug, which one is more clinical useful?

A

antagonist!

More clinically useful, act post-synaptically at specific receptor subtype

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8
Q

Botulinum toxin*: ____1____ ACh release

Black Widow Spider toxin*: ____2____ ACh release

A
  1. blocks

2. increases

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9
Q

What are the two subtypes of Cholinergic Receptors?

A

Nicotinic Receptors

Muscarinic Receptors

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10
Q

ligand gated, alter ionic permeability are the actions of what type of Cholinergic Receptors?

A

Nicotinic Receptors:

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11
Q

G-protein coupled receptors, alters enzyme activity are the actions of what type of Cholinergic Receptors?

A

Muscarinic Receptors:

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12
Q

Nicotinic Receptors: ?

A

ligand gated, alter ionic permeability

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13
Q

Muscarinic Receptors: ?

A

G-protein coupled receptors, alters enzyme activity

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14
Q

Gq → ____1___ PLC

Gi → ___2____ AC

A
  1. increase

2. decrease

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15
Q

What [M] subtype is associated with Gq and what type of cell/organs are they on?

A

M1 = neuronal, GI glands

M3 = exocrine glands, smooth muscle

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16
Q

What [M] subtype is associated with Gi and what type of cell/organs are they on?

A

M2, M4 = heart, CNS

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17
Q

What are the direct acting Muscarinic Cholinergic Receptor Agonists?

A

Choline Esters:

  • Acetylcholine*: not used, rapid hydrolysis by AChE
  • Bethanechol*: synthetic analog of ACh, resistant to AChE

Parasympathetic Alkaloids:
- Pilocarpine*

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18
Q

What are the Nicotinic Neuronal (ganglionic) Receptor Agonists

A
  • Nicotine* → increase BP, HR, vasoconstriction, increase GI motility, arousal, euphoria, increased attention
    Prolonged or toxic dose can cause antagonism due to persistent depolarization → renders membrane unresponsive
  • Acetylcholine*
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19
Q

What is the MOA of Muscarinic Cholinergic Receptor Antagonists?

A

antagonize ACh, reversible (competitive) inhibitors (aka anticholinergic and antimuscarinic)

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20
Q

What are the Muscarinic Cholinergic Receptor Antagonists?

A 
Alkaloids:
     - Atropine*
     - Scopolamine*
Semi-Synthetic Agents: higher selectivity of antagonism particularly parasympathetic function (bladder especially).
     - Oxybutynin*, Ipratropium*
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21
Q

What is the overall MOA of Acetylcholinesterase Inhibitors?

A

Indirect agonist?

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22
Q

List the Acetylcholinesterase Inhibitors. (4)

A
  • Physostigmine
  • Neostigmine, Pyridostigmine
  • Edrophonium
  • Organophosphates (nerve gas, insecticides) act indirectly to inhibit acetylcholine esterase → too much acetylcholine
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23
Q

nerve gas, insecticides are what type of Acetylcholinesterase Inhibitors?

A

Organophosphates

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24
Q

List the adrenergic agonist drugs:

A
  • Epinephrine
  • Pseudoephedrine
  • Norepinephrine
  • Phenylephrine
  • Clonidine
  • Isoproterenol
  • Albuterol
  • Dobutamine
  • Dopamine
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25
Q

List the adrenergic antagonist drugs:

A
  • Doxazosin
  • Propranolol, Timolol = Non-selective B1 and B2
  • Metoprolol, Atenolol = B1 cardioselective (only at lower doses)
  • Labetalol, Carvedilol
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26
Q

What adrenergic antagonist drug is non-selective for beta1 and beta 2?

A

Propranolol, Timolol

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27
Q

What adrenergic antagonist drug is beta1 cardio-selective? (only at lower doses)

A

Metoprolol, Atenolol

28
Q

What part of the CNS does: Reflex changes in blood pressure, sweat production and micturition.

A

Spinal cord

29
Q

What part of the CNS does: Centers for control of blood pressure and respiration

A

Medulla oblongata

30
Q

What part of the CNS does: Principal locus of integration; controls body temperature, water balance, carbohydrate metabolism, sexual reflexes, emotional responses.

A

Hypothalamus

31
Q

What part of the CNS does: Volitional changes and conditioned autonomic responses.

A

Cerebral cortex

32
Q

Sympathetic neurons release what NT in the effector organs?

A

NE

33
Q

What is the neurotransmitter at the sympathetic ganglion?

A

acetylcholine (ACh)

34
Q

What is the NT at the parasympathetic ganglion?

A

ACh

35
Q

Parasympathetic neurons release what NT in the effector organs?

A

ACh

36
Q

What branch of the ANS innervates blood vessels?

A

SNS ONLY!

37
Q

Predominant (basal) tone exerted by which branch of the ANS?

A

PNS

38
Q

Responses directed to single organ system –> ___?___ activation produces discrete, localized discharges

A

PNS

39
Q

What are the physiologic responses in “Rest and Digest” for the:

  • CV
  • GI
  • Bladder and Rectum
  • Pupil
A
  • Slowing of heart rate –> decreased blood pressure.
  • Stimulation of GI motility and secretions.
  • Emptying of bladder and rectum.
  • Pupil constriction - focus (accommodation) for near vision.
40
Q

TRUE or FALSE?

Nicotinic receptors can be found at Bronchial smooth muscle?

A

FALSE!!!

Nicotinic receptors can be found at all of the following sites:

  • Adrenal medullary cells
  • Parasympathetic ganglia
  • Skeletal muscle end plates
  • Sympathetic ganglia
41
Q

Activation of [M] receptors in the CV results in what?

A

Decreased heart rate and AV conduction rate, reduced atrial contractility

Vasodilation - indirect effect mediated via generation of nitric oxide, then cGMP –> decreased blood pressure

NOTE: These muscarinic receptors are NOT innervated - activation of the PNS does NOT result in vasodilation.

42
Q

Activation of [M] receptors in the Respiratory system results in what?

A

Respiratory: Bronchial muscle contraction, stimulation of glands

43
Q

Activation of [M] receptors in the GI Tract results in what?

A

GI Tract: Increase in secretory and motor activity - most sphincters relaxed

44
Q

Activation of [M] receptors in the GU Tract results in what?

A

Genitourinary tract: Relax sphincter muscles, contract detrusor muscle, thus promote voiding.

45
Q

Activation of [M] receptors in the Eye results in what?

A

Contraction of circular muscle  miosis (pupil constriction)

Ciliary body focuses lens for near vision  accommodation

Outflow of aqueous humor (tension on trabecular meshwork increases flow into Canal of Schlemm)   IOP

46
Q

Which of the following drugs causes vasodilation that can be blocked by atropine?

Metoprolol
Bethanechol
Doxazosin
Labetalol
Nitroglycerin
A

Bethanechol

47
Q

[N_N] receptor activation in the ganglia results in what?

A

Cardiovascular: Chiefly sympathetic effects - moderate vasoconstriction, tachycardia, elevated blood pressure

GI / urinary tract: Parasympathetic effects = nausea, vomiting, diarrhea, urination

48
Q

[N_N] receptor activation in the CNS results in what?

A

Mild alerting effect, tremor, emesis, respiratory stimulation

Activates “reward” pathway in limbic system contributing to addiction potential

Convulsions can occur at toxic doses

49
Q

“Fight or Flight”/SNS activation does what to:

  • HR/BP
  • blood flow/management
  • bronchioles/pupils
  • blood glucose
A
  • Accelerated heart rate = increased blood pressure
  • Shift of blood from skin-splanchnic regions to skeletal muscles
  • Dilation of bronchioles and pupils
  • Rise in blood glucose
50
Q

What adrenergic receptors are at cutaneous, mucous membranes, splanchnic vessels and what is the physiological results?

A

Cutaneous, mucous membranes, splanchnic vessels = [Alpha-1]

Vasoconstriction mediated via 1 receptors, contributes significantly to increase in total peripheral resistance

51
Q

What adrenergic receptors are at Skeletal muscle vasculature and what is the physiological results?

A

Skeletal muscle vasculature = [Alpha-1 and Beta-2]

Vasoconstriction (Alpha-1) or vasodilation (Beta-2) can occur

Beta-2 receptor activation increases blood flow to muscle and decreases total peripheral resistance

52
Q

What adrenergic receptors are at Renal vasculature and what is the physiological results?

A

Renal vasculature = [D1 and Alpha-1]

Vasodilation via D1 receptors balanced by constriction via α1 receptors (dose-dependent effect of dopamine)

53
Q

What adrenergic receptors are at Heart and what is the physiological results?

A

Direct effects on heart are largely mediated by [Beta-1] receptors

SA node: Increase in heart rate (positive chronotropy)

AV node: Increase in conduction velocity

Atrial - ventricular cardiac muscle: Increase in force of contraction (positive inotropy)

54
Q

What adrenergic receptors that control Blood Pressure and what are the physiological results?

A

α1: Vasoconstriction –> increase TPR and BP –> reflex bradycardia occurs.

β1: Increased heart rate / force of contraction –> increase CO and BP.

β2: Vasodilation –> decreases TPR and BP –> reflex tachycardia occurs.

55
Q

What adrenergic receptors are in JGA cells (kidney) and what is the physiological results?

A

Juxtoglomerular cells: Increased renin release via [α1] receptors.

56
Q

What adrenergic receptors are at the Respiratory Tract and what are the physiological results?

A

Respiratory Tract:

Bronchial smooth muscle: Bronchodilation via [β2] receptors.

Upper respiratory tract mucosal blood vessels: Constriction via [α1] receptors.

57
Q

What adrenergic receptors are in the GI tract and what is the physiological results?

A

Gastrointestinal Tract: Smooth muscle

Indirect relaxation via presynaptic [α2] receptors inhibiting release of ACh and ACh-mediated muscle contraction.

Direct relaxation via by [β2] - [β3] receptors on smooth muscle.

58
Q

What adrenergic receptors are at Uterine smooth muscle and what is the physiological results?

A

Uterine smooth muscle: Relaxation via [β2] receptors.

59
Q

What adrenergic receptors are at Uretal sphincter and what is the physiological results?

A

Uretal sphincter, bladder base, prostate: Contraction via α1 receptors –> Increase continence.

60
Q

What adrenergic receptors are at bladder wall musculature and what is the physiological results?

A

Bladder wall musculature: Relaxation via [β2]-[β3] receptors promoting urinary continence.

61
Q

What adrenergic receptors for ejaculation and what is the physiological results?

A

Ejaculation: Via α1 receptor activation in vas deferens, seminal vesicles, and prostate.

62
Q

What adrenergic receptors for the radial pupillary dilator muscle and what is the physiological results?

A

Radial pupillary dilator muscle: Constriction via [α1] receptors –> mydriasis (dilation).

63
Q

Aqueous humor –> intraocular pressure (IOP) - balance between production and outflow)

Major effect: Increased production via ___1___ receptors (increases IOP)

Minor effect: Increased outflow via ___2___ receptors vasoconstriction of ocular vessels (decreases IOP)

A
  1. beta receptors

2. Alpha-1 receptors

64
Q

What adrenergic receptors are in skeletal muscle and what is the physiological results?

A

Skeletal Muscle [β2]

[β2] receptors located on extrafusal fibers and muscle spindles.

Activation associated with marked tremor - dose-dependent enhancement of muscle spindle discharge.

65
Q

Liver: Increased glycogenolysis via what adrenergic receptors –>increased blood glucose

A

[β2]

66
Q

Fat cells: Increased lipolysis (fat breakdown) via what adrenergic receptors?

A

[β3]

67
Q

Pancreas β cells

Decreased insulin secretion via what adrenergic receptors? (major effect)

Increased insulin release via what adrenergic receptors?

A

Pancreas β cells

Decreased insulin secretion via [[α2] receptor (major effect).

Increased insulin release via [β2] receptors.

NS_BTRAN (21 decks)

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