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CV exam 2 > Intro to ANS pharm > Flashcards

Intro to ANS pharm Flashcards

1
Q

what is an agonist?

A

activate the receptor to signal as a direct result of binding to it

some agonists activate a receptor to produce all of the receptor’s biologic functions

some agonists selectively promote one receptor function more than another

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2
Q

what is an antagonist?

A

bind to receptors but do not activate generation of a signal

interfere with the ability of an agonist to activate the receptor

some antagonists suppress the basal signaling of receptors that are constitutively active

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3
Q

what is the sympathetic response of the ANS

A

fight or flight

thoracolumbar location

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4
Q

what is the parasympathetic response

A

rest and digest

craniosacral

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5
Q

what is the major NT of parasympathetic NS

A

ACh

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6
Q

what are the major receptors in the parasympathetic pathway

A

nicotinic AChr (found at all postganglionic nerves)

muscarinic AChR (found on all smooth muscle in the parasympathetic NS)

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7
Q

what are the two exceptions to the normal rules of sympathetic and parasympathetic innervation and NT’s

A

sweat glands
-main receptor is muscarinic
and the main NT is ACh
this is a sympathetic response

adrenal medulla
-main receptor is nicotinic
and the main NT is ACh
this is a sympathetic response

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8
Q

what is adrenergic?

A

Sympathetic nervous system

“adrenaline” fight or flight

usually involves beta and alpha receptors

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9
Q

what is cholinergic

A

parasympathetic nervous system

usually involves the nicotinic and muscarinic receptors

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10
Q

what is the major NT of the parasympathetic NS

A

Acetylcholine

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11
Q

where is ACh found

A

All preganglionic autonomic fibers
All postganglionic parasympathetic fibers
Few postganglionic sympathetic fibers (sweat glands–> ACh activating muscarinic receptors in the sympathetic ns)

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12
Q

what is the significance of norepinephrine

where is its location

A

The major neurotransmitter of the sympathetic nervous system
The vast majority of postganglionic sympathetic fibers

it is a catecholamine

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13
Q

where is epinephrine synthesized

A

Synthesis only occurs in the adrenal medulla and in a few epinephrine-containing neuronal pathways in the brainstem

epinephrine is a catecholamine

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14
Q

what is dopamine a precursor for

and what is dopamines function

A

NE and Epi precursor
Acts on the CNS and renal vascular smooth muscle

dopamine is a catecholamine

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15
Q

WHAT are the steps in cholinergic neurotransmission?

A 
1 Junctional transmission
 Synthesis of acetylcholine (ACh)
 Storage
 Release
 Destruction (reuptake)

2 ACh signaling

3 End organ effects

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16
Q

what is the function of nicotinic receptors?

A

excitatory

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17
Q

what is the function of muscarinic receptors

A

excitatory or inhibitory

sweat excretion

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18
Q

Norepinephrine location

A

principal NT of most sympathetic postganglionic fibers and of certain tracts in the CNS

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19
Q

how does tyrosine get into the nerve terminal?

A

sodium dependent transporter

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20
Q

why is sodium ECF important?

A

because of transport of tyrosine (for catecholamine synthesis)
and because of transport of choline into the nerve terminal to make ACh

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21
Q

what is the order of synthesis of catecholamines

A 
tyrosine
dopa
dopamine
norepinephrine
epinephrine

(tyrosine to dopamine in nerve cytoplasm)
NE to Epi in the adrenal medulla

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22
Q

why is cocaine a sympathetic stimulant?

A

because it blocks the reuptake of NE back in to the nerve terminal remaining there longer, leading to increased sympathetic output

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23
Q

VMAT-2

A

Transports NE, Epi, DA, and serotonin into vesicles (promiscuous)

Release upon action potential and Ca2+ influx

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24
Q

what does resperine do?

A

blocks VMAT-2 (transporter)

decreased amount of NE stored in the vesicle
decreased amount of NE when released activates less alpha and beta receptors
now have decreased sympathetic tone and decreased blood pressure
but not a good drug b/c it was not very selective

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25
Q

what does NET do?

DAT?

A

imports NE into the nerve terminal

DAT transports dopamine

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26
Q

metabolism of catecholamines occurs via what 2 enzymes?

A

MAO

COMT

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27
Q

in contrast to cholinergic signaling, termination of catecholamine action by degradative enzymes (i.e.. AChe) is….

A

is nonexistent in adrenergic signaling

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28
Q

is there parasympathetic innervation to the smooth muscle that surrounds the vasculature?

A

NO

so no opposite response

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29
Q

what is the role of ACh and muscarinic agonist given IV?

A

cause vasodilation due to release of NO

30
Q

what does NO do? what type of patient is this good for?

A

causes vasodilation

for someone having a heart attack this is good because it dilates vessels around the heart, leading to increased perfusion

31
Q

what are the agonists for alpha 1

what is the result of ligand binding to alpha 1

A

Epi ≥ NE&raquo_space; Iso
Phenylephrine

Formation of IP3 and DAG, increased intracellular Ca2+

32
Q

what is the end result of alpha 1 activation

A 
Contraction
vasoconstriction
Glycogenolysis; 
gluconeogenesis
Hyperpolarization and 
relaxation (in the gut)
Increased contractile force; arrhythmias
33
Q

what tissue is alpha 1 usually in

A 
Vascular, 
GU smooth muscle
Liver
Intestinal smooth muscle 
Heart
34
Q

alpha 1 known for….

A

smooth muscle contraction

35
Q

alpha 2 known for its function in…

A

presynaptic

vascular smooth muscle contraction
decreased insulin production
decreased release of NE

36
Q

alpha 2 agonists

result of ligand binding to alpha 2

A

Epi ≥ NE&raquo_space; Iso
Clonidine

ligand binding causes inhibition of adenyl cyclase and decreased cAMP

37
Q

tissue location of alpha 2

A

Pancreatic islets (β cells)
Platelets
Nerve terminals
Vascular smooth muscle

38
Q

Beta 1 primary location

A

heart

juxtaglomerular cells

39
Q

beta 1 agonists

A

Iso > Epi = NE

Dobutamine

40
Q

result of ligand binding to beta 1

A

stimulation of adenyl cyclase

increased cAMP

41
Q

end result/function of beta 1

A

Increased renin secretion

Increased force and rate of contraction and AV nodal conduction velocity

42
Q

beta 2 agonists

A

Iso > Epi&raquo_space; NE

Terbutamine

43
Q

beta 2 location

A 
Smooth muscle (vascular, BRONCHIAL, GI, GU)
Skeletal muscle
44
Q

beta 2 function/outcome

A

Relaxation of smooth muscles- vascular, bronchial, genitourinary, gastrointestinal

Vasodilation/bronchiodilation

Glycogenolysis;
uptake of K+

USED IN ASTHMA

45
Q

beta 3 agonists

A

Iso = NE > Epi

46
Q

location of beta 3 and outcome of beta 3 activation

A

adipose tissue

lipolysis

47
Q

where is the location of M2 (muscarinic)

A

primarily found in heart

48
Q

what is the outcome of activation of M2 receptors

A

slows down heart rate

inhibition of cAMP production activation of K+ channels

49
Q

where is the primary location of the M3 receptors

A

Glands, smooth muscle, endothelium

smooth muscle surrounding organs in the parasympathetic NS

50
Q

what is the function of M3

A

constriction of lungs

does so by….
IP3, DAG cascade
-increased Ca to cause muscle contraction

51
Q

what are alpha 1 blockers used for?

A

high blood pressure

52
Q

what percentage of catecholamine release from the adrenal medulla is NE and how much Epi

A

80 % epi

20 % NE

53
Q

what causes the release of epi and nE

A

triggered by the release of ACh from preganglionic fibers

Ach binds to Nicotinic ACh receptors and produces a localized depolarization

54
Q

what type of receptor are the dopamine receptors?

A

GPCR’s

55
Q

what is the result of Dopamine activating D1 receptors. Where are D1 receptors

A

D1 receptors are on renal smooth muscle

it causes increases cyclic AMP and causes dilation

vasodilation, natriuresis, and diuresis via renal vascular smooth muscle

56
Q

what can dopamine at higher concentrations activate? and what would be the outcome of this

A

can activate alpha 1 and beta 1 receptors to cause and increase in heart rate and general vasoconstriction

57
Q

what is necessary to have vascular relaxation in response to ACh?

A

an intact epithelium (endothelium)

b/c when ACh activates mAChR’s on endothelial cells NO is subsequently produced by the endothelial cells where it diffused back to the smooth muscle cells surrounding blood vessels and causes relaxation

58
Q

what is the primary controlled variable in cardiovascular function

A

MAP

59
Q

what are cholinomimetic agents

A

drugs that mimic ACh

AChR agonists
Acetylcholiesterase inhibitors (keeps ACh in cleft longer)
60
Q

what are cholinoceptor blocking drugs?

A

AChR antagonists

61
Q

what are sympathomimetic agents

A

drugs that mimic or enhance alpha and beta receptor stimulation

Agonists–> drugs that enhance catecholamine release, drugs that block reuptake

62
Q

what are adrenoceptor blocking drugs

A

alpha and beta receptor antagonists

63
Q

what are two examples of agents/drugs that interfere with NT synthesis

A

ChAT inhibitors (so can’t make ACh)

alpha-methyltyrosine (blocks tyrosine hydroxylase) so can’t make tyrosine to Dopa

this causes depletion of NE and minimal depletion of ACh

64
Q

what are two examples of agents that inhibit NT storage?

A

Vesamicol–> cholinergic
-blocks ACh storage

Resperpine–> adrenergic
-blocks NE storage and depletion by MAO so it slows the parasympathetic output

65
Q

what does botulinum toxin do

A

it is an anticholinergic and blocks NT release

66
Q

what does bretylium and guanadrel do?

A

antiadrenergic by blocking the release of NT

67
Q

what does hemicholinium do?

A

blocks choline uptake and causes subsequent ACh depletion

inhibition of NT reuptake

68
Q

what does cocaine do?

A

blocks transport of NE

so there is a buildup of NE and prolongs adrenergic effects

69
Q

what do AChE inhibitors do?

A

cause ACh accumulation at the synapse

so that means there is a prolonged symapthetic response

70
Q

what do MAO inhibitors cause?

A

catecholamine accumulation in the nerve terminal because normally MAO metabolizes catecholamines that have been released and undergone reuptake within the nerve terminal

CV exam 2 (4 decks)

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