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Principles > Autonomic Pharmacology > Flashcards

Autonomic Pharmacology Flashcards

1
Q

What is depolarisation?

A

A decrease in membrane potentail

Becomes less negative

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2
Q

What is hyperpolarisation?

A

An increase in membrane potential

Becomes more negative

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3
Q

In which direction will sodium move in response to the opening of cell membrane sodium selective channels, and why?

A

Into the cell
Concentration gradient is inward
Electrical gradient is inward

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4
Q

In which direction will potassium move in response to the opening go cell membrane potassium selective channels, and why?

A

Out of the cell
Concentration gradient is outward
Electrical gradient is inward, but of an energy less than the concentration gradient

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5
Q

What is the effect of opening sodium selective channels on the membrane potential?

A

Depolarisation

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6
Q

What is the effect of opening potassium selective channels on the membrane potential?

A

Hyperpolarisation

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7
Q

What are action potentials?

A

Brief electrical signals in which the polarity of the nerve cell membrane is momentarily reversed

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8
Q

How is the activation of sodium channels controlled?

A

Self-reinforcing
Positive feedback
Opening of a few causes further channels to open and so on

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9
Q

How is the activation of potassium channels controlled?

A

Self-limiting
Negative feedback
Outward movement of potassium causes depolarisation which turns off the stimulus for opening

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10
Q

What activates the opening of sodium and potassium channels?

A

Membrane depolarisation
Sodium channel open rapidly
Potassium channel open with slight delay

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11
Q

What is the absolute refractory period?

A

No stimulus, however strong, can elicit a second action potential
All sodium channels are inactivated
DOWNSTROKE

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12
Q

What is the relative refractory period?

A

A stronger than normal stimulus may elect a second action potential
Mixed population of activated/inactivated sodium channels
UNDERSHOOT

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13
Q

What are the phases of an action potential?

A 
Resting potential 
Threshold 
Upstroke 
Overshoot 
Downstroke 
Undershoot
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14
Q

Why is the conduction of APs in myelinated axons much faster than in nonmyelinated axons of the same diameter?

A

Myelin acts as an insulator to prevent “leakiness” from the axon

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15
Q

What causes the undershoot in an action potential?

A

Delayed closure of voltage activated potassium channels

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16
Q

In which three conformations do sodium channels exist?

A

Open
Closed
Inactivated

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17
Q

What is the overall function of the autonomic nervous system?

A

Carries output from CNS to the whole of the body (not skeletal muscle)
Regulates visceral functions that are largely involuntary
Subdivided into sympathetic and parasympathetics

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18
Q

What are the neurotransmitters involved in sympathetic neurones?

A 
Preganglionic neurone (cholinergic)  = 
Acetylcholine 
Postganglionic neurone (usually adrenergic) = 
Noradrenaline (usually)
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19
Q

What are the neurotransmitters and receptors involved in parasympathetic neurones?

A

Preganglionic and postganglionic neurone =
NT Acetylcholine
R Cholinergic

20
Q

Give an overview of neurochemical transmission?

A

Uptake of precursor into nerve terminal
Synthesis and storage of transmitter
Depolarisation of nerve terminal by action potential stimulated calcium influx
Calcium influx induces release of transmitter by exocytosis
Transmitter synapses across and activates receptors on post synaptic cell
Enzyme mediated inactivation of transmitter, or reputed of transmitter

21
Q

Explain chemical transmission in the sympathetic division?

A

AP travels to presynaptic terminal triggering calcium entry and release of ACh
ACh opens ligand-gated ion channels (nictonic ACh receptors) on postganglionic neurone, causing AP
AP travels to presynaptic terminal triggering calcium entry and release of noradrenaline
Noradrenaline activates G-protein-coupled adrenoceptors in target cell

22
Q

Explain chemical transmission in the parasympathetic division?

A

AP travels to presynaptic terminal triggering calcium entry and release of ACh
ACh opens ligand-gated ion channels (nictonic ACh receptors) on postganglionic neurone, causing AP
AP travels to presynaptic terminal triggering calcium entry and release of ACh
ACh activates G-protein-coupled muscarinic acetylcholine receptors in target cell

23
Q

What is the composition of ligand gated ion channels and how does this relate to rate of signalling?

A

Consist of separate glycoprotein subunits with a central ion conducting channel
Allows rapid changes to membrane permeability to ions and rapidly alters membrane potential

24
Q

What is the composition of G-protein-coupled receptors and how does this relate to rate of signalling?

A

Receptor, G protein and effector are separate proteins
G protein ats as an intermediate between the receptor and the effector
Signalling is much slower than ligand gated ion channels

25
Q

What is the basic structure of the G-protein-coupled receptor?

A

Integral membrane protein
Extracellular NH2
Intracellular COOH termini

26
Q

What is the basic structure of the G protein?

A

Peripheral membrane protein
Three polypeptide subunits (alpha, beta, gamma)
Beta and gamma form a subunit which never dissociates
The alpa sub unit can dissociate during signalling, and can bind GDP or GTP

27
Q

Explain how G-protein-coupled receptors work to turn on the signal?

A

Agonist activates receptor
G protein couples with receptor
GDP disscoates from and GTP binds to the alpha subunit
G protein dissociated into its two subunits
Alpha subunit combines with and modifies activity of effector
Agonist may dissociate from receptor, but signalling can persist

28
Q

Explain how G-protein-coupled receptors work to turn off the signal?

A

Alpha subunit acts as an enzyme to hydrolyse GTP to GDP and Pi
Signal is turned off
Alpha subunit recombines with beta-gamma subunit

29
Q

How many subunits does a Nicotinic ACh Receptor consist of?

A

Five glycoprotein subunits

30
Q

What are the main types of peripheral nicotinic ACh receptors and what is their structure?

A 
Skeletal muscle = 
2 Alpha 1
Beta 1
Gamma 
Beta/delta

Ganglionic =
3 Alpha
2 Beta

31
Q

How many molecules of ACh need to bind to the peripheral nicotinic ACh receptors to open them?

A

Two

32
Q

Explain cholinergic transmission at pre/postganglionic junction?

A

Uptake of choline via transporter
Synthesis of ACh via CAT
Storage of ACh via transporter in concentrated vesicle
Depolarisation by action potential
Calcium influx
Calcium induced release of ACh by exocytosis
Activation of ACh receptors causing cellular response
Degradation of ACh to choline and acetate by AChE terminates transmission
Reuptake and reuse of choline

33
Q

How does cholinergic transmission at a ganglia elict an AP?

A

The more ACh that is reaeased, the greater the depolarisation
As long as the amplitude of excitatory post synaptic potential is big enough, voltage activated sodium channels are opened
This causes further action potentials

34
Q

What drugs affect cholinergic transmission at ganglia?

A

Non of any current clinical significance
Nicotine
Hexamethonium - First antihypertensive, no longer used

35
Q

How is cholinergic transmission at a parasympathetic neuroeffector junction different to that at the pre/postganglionic junction?

A

Release of ACh activates muscarinic ACh receptor subtypes (M1-M3) causing cellular response

36
Q

Explain noradrenergic transmission at sympathetic neuroeffector junctions?

A

Synthesis of NA
Storage of NA by transporter in vesicles
Depolarisation by AP
Calcium influx through voltage gated channels
Calcium induced release of NA
Activation of adrenoceptor subtypes causing cellular response
Reuptake of NA by transporters U1 and U2
Metabolism of NA by MAO and COMT

37
Q

How is the release of neurotransmitters regulated at neuroeffector junctions?

A

By presynaptic autoreceptors by negative feedback mechanisms
Both ACh and NA regulate their own release

38
Q

How does cocaine affect the autonomic nervous system?

A

Blocks U1 receptors (and so blocks reuptake of NA)
NA concentration in the synaptic cleft increases
Increased stimulation of effector cell adrenoceptors

Causes vasoconstriction (increased BP) and cardiac arrhythmias

39
Q

How does amphetamine affect the autonomic nervous system?

A

Substrate for U1, enters noradrenergic terminal and inhibits MAO, enters vesicle and displaces NA into the cytoplasm
NA exits the terminal on U1, accumulates in the synaptic cleft and increases effector cell adrenoceptor stimulation

Causes vasoconstriction (increased BP) and cardiac arrhythmias

40
Q

How does prazosin affect the autonomic nervous system?

A

Selective competitive antagonist of alpha 1 adrenoceptor

Vasodilator used as an antihypertensive

41
Q

How does atenolol affect the autonomic nervous system?

A

Selective competitive antagonist of beta 1 adrenoceptors

Anti-anginal and antihypertensive use

42
Q

How does salbutamol affect the autonomic nervous system?

A

Selective agonist of beta 2 adrenoceptors

Used as bronchodilator

43
Q

How does atropine affect the autonomic nervous system?

A

Competitive antagonist of muscarinic ACh receptors
Exerts widespread effects by blockade of the parasympathetic division of ANS
Used to reverse bradycardia following MI and in anticholinesterase poisoning

44
Q

What are the three main subtypes of muscarinic receptors at parasympathetic neuroeffector junctions?

A

M1 - stimulates phospholipase C (stomach)
M2 - inhibits adenylyl cyclase, opens potassium channels (heart)
M3 - stimulates phospholipase C (salivary glands, smooth muscle)

45
Q

What are the four main subtypes of adrenoceptors at sympathetic neuroeffector junctions?

A

Beta 1 - stimulates adenylyl cyclase (heart)
Beta 2 - stimulates adenylyl cyclase (smooth muscle)
Alpha 1 - stimulates phospholipase C (vascular smooth muscle)
Alpha 2 - Inhibits adenylyl cyclase

Principles (13 decks)

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