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year 1 foundations > autonomic pharmacology > Flashcards

autonomic pharmacology Flashcards

1
Q

what are the 3 divisions of the autonomic nervous system (ANS)?

A
  • enteric
  • sympathetic
  • parasympathetic
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2
Q

what are the functions of the ANS?

A

= regulates functions essential to human health and life that do not require conscious effort (e.g. whilst asleep) and that are largely involuntary:
1. contraction and relaxation of vascular and visceral smooth muscle
2. the heartbeat (including rate and force)
3. all exocrine and certain endocrine secretions
4. aspects of metabolism (particularly in liver and skeletal muscle)
5. modulation of the processes of the immune system

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3
Q

what is the transmitter of preganglionic neurons?

A

ALWAYS acetylcholine acting via excitatory nicotine cholinoceptors
(released by preganglionic to act on post ganglionic)

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4
Q

what is usually transmitter of postganglionic neurons for
a) sympathetic?
b) parasympathetic?

A

a) noradrenaline
b) acetylcholine
(released by post ganglionic to act on effector cell)

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5
Q

describe the chemical transmission of sympathetic division?

A
  • travels to the presynaptic terminal of the preganglionic neuron triggering Ca2+ entry through voltage-gated, calcium selective, ion channels and the release of ACh by exocytosis
  • ACh binds to and opens ligand-gated ion channels (nicotinic ACh receptors) in the postganglionic neuron, causing depolarization and the initiation of action potentials that propagate to the presynaptic terminal of the neuron, triggering Ca2+ entry and the release, usually, of noradrenaline
  • noradrenaline activates G-protein-coupled adrenoceptors in the effector cell membrane to cause a cellular response via ion channels/enzymes
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6
Q

how does the chemical transmission of parasympathetic division compare to sympathetic division?

A

= very similar to sympathetic pathway except:

  • acetyl choline is always the classical transmitter used by postganglionic neurons
  • acetyl choline activates G protein coupled muscarinic acetylcholine receptors in the effector cell membrane to cause a cellular response via ion channels/ enzymes
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7
Q

are ACh and NA the only transmitters released from sympathetic & parasympathetic postganglionic fibres?

A

NO - sometimes NANC transmission
= more frequently though, NA & ACh are co-released with NANC c-transmitter/modulator

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8
Q

what is NANC transmission?

A

non-adrenergic & non-cholinergic transmission (when not ACh or NA)

  • commonly released as co-transmitter alongside NA & ACh
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9
Q

what are some transmitters of sympathetic?

A

noradrenaline = dominant transmitter
fine-tuning = ATP and neuropeptide Y (NPY)

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10
Q

what are transmitters for parasympathetic?

A

dominant = acetyl choline
fine-tuning = nitric oxide (NO) and vasoactive intestinal peptide (VIP)

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11
Q

what are the rapid response neurotransmitters for sympathetic & parasympathetic?

A

parasympathetic = Ach
sympathetic = ATP

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12
Q

what are the intermediate response neurotransmitters (medium response time) for sympathetic & parasympathetic?

A

parasympathetic = NO (nitric oxide)
sympathetic = noradrenaline

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13
Q

what are the slow response neurotransmitters for sympathetic & parasympathetic?

A

parasympathetic = VIP (vasoactive intestinal peptide)
sympathetic = NPY (neuropeptide Y)

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14
Q

what is acetyl choline?

A

endogenous agonist of cholinoceptors that are nicotinic or muscarinic

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15
Q

what is effect of influx of calcium ions?

A

stimulates exocytosis (amongst other things)

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16
Q

what are nicotinic ACh receptors of ganglia?

A
  • Ligand-gated ion channels (LGICs),selectively activated by the plant alkaloid, nicotine
  • Structurally and pharmacologically distinct from nicotinic receptors at the skeletal neuromuscular junction, or in the CNS
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17
Q

what are muscarinic ACh receptors of ganglia?

A
  • G-protein-coupled receptors (GPCRs), selectively activated by the plant alkaloid,muscarine
  • Structurally and pharmacologically defined as five subtypes: M1, M2, M3, M4 and M5 that are differentially expressed across tissues/organs, M1-3 being most important in the ANS
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18
Q

what receptor stimulation causes increased heart rate & increased force of contraction in atria & ventricles

A

sympathetic stimulation of beta 1 adrenoceptors

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19
Q

what type of receptor mostly stimulates
a) sympathetic?
b) parasympathetic?

A

a) adrenoceptors
b) muscarinic cholinoceptors

20
Q

what receptor stimulation causes relaxation of bronchi & decrease mucus production (decreased airway resistance)?

A

sympathetic stimulation of beta 2 adrenoceptor

21
Q

what receptor stimulation causes reduced intestinal motility & constriction of sphincters?

A

sympathetic stimulation of alpha 1 & 2 and beta 2 adrenoceptors

22
Q

what receptor stimulation causes constriction of vasculature in most locations but relaxation in skeletal muscles?

A

sympathetic stimulation - constriction of vasculature by alpha 1 adrenoceptor and relaxation of skeletal muscle by beta 2

23
Q

what receptor stimulation causes release of adrenaline from adrenal medulla?

A

sympathetic stimulation of nicotinic ACh receptor

24
Q

what receptor stimulation causes relaxation of wall of bladder and constriction of internal sphincter?

A

sympathetic stimulation - relaxed wall = beta 2 & 3 adrenoceptor - constriction of internal sphincter = alpha 1 adrenoceptor

25
Q

what receptor stimulation causes ejaculation?

A

sympathetic stimulation = alpha 1 adrenoceptor

26
Q

what receptor stimulation causes decreased heart rate & force in atria?

A

parasympathetic stimulation - M2 muscarinic cholinoceptor

27
Q

what receptor stimulation causes constriction of bronchioles and stimulates mucus production (increasing airway resistance)?

A

parasympathetic stimulation - M3 muscarinic cholinoceptor

28
Q

what receptor stimulation causes increased intestinal motility & secretions and relaxation of sphincters?

A

parasympathetic stimulation - M3 muscarinic cholinoceptor
(nitric oxide (NO) also relaxes sphincters)

29
Q

what receptor stimulation causes contraction of bladder walls and relaxes internal urethral sphincter?

A

parasympathetic division - M3 contracts wall and NO relaxes internal sphincter

30
Q

what do cholinergic fibres release?

A

acetyl choline as transmitter - activated cholinoceptors
(parasympathetic - has mostly muscarinic cholinoceptors and always releases ACh by post ganglionic neurons)

31
Q

describe process and general features of cholinergic transmission?

A
  1. uptake of choline via transporter (rate limiting synthesis of ACh)
  2. choline + AcCoA - synthesis of ACh by choline acetyltransferase (ChAT)
  3. storage of ACh within vesicle via transporter (VASChT). ATP & other anions are co-stored
  4. depolarization of the terminal by action potential
  5. influx of Ca2+ through voltage gated channel
  6. Ca+ induce release of ACh from vesicles (exocytosis)
  7. activation of ACh receptors (nicotinic or muscarinic) causing cellular response
  8. degradation of ACh to cheloine & acetate
  9. reuptake & reuse of choline
32
Q

what is composition of nicotinic acetylcholine receptor?

A

composed of multiple subunits (5) that surround centrally located ion channel - cation conducting (Na+, K+, Ca 2+)

  • there’s lots of different subtypes that all have different combination of subunits which influences the permeability of certain ions
33
Q

what is EPSP and what does it lead to?

A

EPSP = excitatory post synaptic potential

  • if reaches threshold then triggers activation of voltage gated Na+ channels which open up and lead to influx of Na+ making action potential
34
Q

what is an open channel blocker? and how is a blockage achieved?

A

non-competitive inhibition = receptors are activated but channel blocker prevents ions from moving through

blockage achieved by:
- depolarisation by high concentrations of agonists
- competitive anatagonism
- non-competitive antagonism

35
Q

what is process of cholinergic transmission at parasympathetic neuroeffector junction?

A
  1. depolarization by action potential
  2. Ca2+ influx through voltage gated channels
  3. Ca+ influx induces release of ACh by exocytosis
  4. activation of muscarinic ACh receptor subtypes (M1-3) causing cellular response (tissue dependant)
  5. degradation of ACh to choline & acetate by acetylcholinesterase - terminates transmission
  6. reuptake & reuse of choline
36
Q

what happens when muscarinic receptor M1 bound by ACh?

A
  • it’s a G-protein coupled receptor so if alpha Gq bound then stimulates phospholipase C and leads to increased acid secretion
37
Q

what happens when muscarinic receptor M2 bound by ACh?

A
  • it’s a G-protein coupled receptor so if alpha Gi bound then inhibits adenylyl cyclase -> opening of K+ channels which eventually decreases heart rate
38
Q

what happens when muscarinic receptor M3 bound by ACh?

A
  • it’s a G-protein coupled receptor so if alpha Gq then stimulation of phospholipase C which increases salivary gland secretion & contraction of bronchioles
39
Q

what is process of noradrenergic transmission at sympathetic neuroeffector junction?

A
  1. synthesis of noradrenaline (multiple steps)
  2. storage of NA by transporter (concentrates)
  3. depolarization by action potential
  4. Ca2+ influx through voltage-gated channels
  5. Ca+ influx induces release of NA by exocytosis
  6. activation of adrenoceptor subtypes causing cellular response (tissue dependant)
  7. reuptake of NA by transporters uptake 1 (U1) and uptake 2 (U2)
  8. metabolism of NA by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT)
40
Q

what is affect of neurotransmitter binding to
a) beta 1 adrenoceptor?
b) beta 2 adrenoceptor?
c) alpha 1 adrenoceptor?
d) alpha 2 adrenoceptor?
(less detail than other flashcard set)

A

a) alpha Gs -> stimulates adenylyl cyclase -> increased rate & force of heart
b) alpha Gs-> stimulates adenylyl cyclase -> relaxation of bronchi & vascular smooth muscle
c) alpha Gq ->stimulation of phospholipase C -> contraction of vascular smooth muscle
d) alpha Gi -> inhibition of adenylyl cyclase -> inhibition of noradrenaline release

41
Q

what mediates negative feedback inhibition of transmitter release?

A

presynaptic autoreceptors (typically leads to a reduction in the further release of neurotransmitters from the presynaptic terminal)

agonists = decrease release (as binds to presynaptic receptor which makes negative modulatory effect of Ca2+ so less ACh released)

antagonists = increase release (as they block the presynaptic receptors so no negative modulatory effect and therefore increase of ACh)

42
Q

what are all the different sites of action drugs can affect cholinergic synapse?

A
  1. directly affecting neurotransmitter release (in presynaptic neuron)
  2. direct agonist/antagonist binding to post-synaptic receptors
  3. inhibition of metabolising enzymes such as AChE inhibitors
  4. uptake inhibitors
43
Q

what affect does cocaine have?

A

in CNS - it blocks reuptake carrier proteins for dopamine & noradrenaline →so increasing amount of noradrenaline - also happens in brain so addictive effect
- it is drug with multiple affinities so can cause problems in lots of places

44
Q

what affect does amphetamine have?

A
  • double whammy effect
  • blocks reuptake of dopamine & noradrenaline & also stimulates release
  • comes in through carrier protein and gets into presynaptic cell
45
Q

what are examples of drugs that are selective competitive antagonists of
a) alpha 1?
b) beta 1 ?

A

a) prazosin
b) atenolol

46
Q

what affect does atropine have?

A

= it’s a competitive antagonist of muscarinic ACh receptors (blocks all muscarinic) , does not block nicotinic ACh receptors

  • therefore exerts widespread effects by blockade of the parasympathetic division of the ANS
    (used to reverse bradycardia following MI)
47
Q

what do each of the horns of the spinal cord contain?

A

dorsal horn = contains sensory nuclei involved in the reception of sensory information from the peripheral nervous system

ventral horn = contains motor nuclei involved in the control of skeletal muscles

lateral horn = contains autonomic nuclei involved in the regulation of involuntary bodily functions (from T1-L2)

*nuclei is name for collection of nerve cell bodies in spinal cord (CNS) in PNS they’re called ganglia

year 1 foundations (36 decks)

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