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QUIZ 7 > Adrenergic Drugs I > Flashcards

Adrenergic Drugs I Flashcards

1
Q

adrenergic receptors are _

A

GPCR’s

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2
Q

alpha-1 receptors

A

Gq phosphorylates alpha subunit –> beta-gamma detach –> Galpha-Pi activates PLC –> PLC cleaves PIP2 into DAG and IP3 (2nd messengers)

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3
Q

alpha-1 receptor functions

A

vasoconstriction, smooth muscle relaxation, contraction of GI tract, increase heart force, and stimulates glygenolysis/gluconeogenesis

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4
Q

muscle contraction by alpha-1 receptors

A

increases intracellular [Ca++] via release of intracellular stores –> calmodulin activation –> phosphorylation of MLCs

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5
Q

alpha-2 receptors

A

activation of Gi

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6
Q

Gi protein

A

inhibits adenylyl cyclase, reducing cAMP; also activates K+ channels for repolarization

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7
Q

alpha-2 receptor functions

A

contraction of smooth muscle, decreases insulin secretion, decreases NE release

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8
Q

beta-receptors

A

activate Gs which activates adenylyl cyclase

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9
Q

beta-1 receptors

A

in heart, kidneys, and adipocytes; produce positive inotropic and chronotropic effect

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10
Q

beta-2 receptors

A

in heart, vascular, bronchial and GI smooth muscle, glands, leukocytes, hepatocytes; smooth muscle relaxation

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11
Q

beta-3 receptors

A

in adipose tissue and GI tract; metabolic effects

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12
Q

beta receptors are found on _

A

post-synaptic cells

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13
Q

alpha-2 receptors are found on _

A

pre or post-synaptic cells

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14
Q

alpha-1 receptors are found on _

A

post-synaptic cells

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15
Q

beta-1 effects

A

tachycardia, increased renin, increased myocardial contractility

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16
Q

beta-2 effects

A

vasodilation, decreased peripheral resistance, bronchodilation, increases glucagon, increases glycogenolysis

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17
Q

signal termination steps

A

desensitization –> sequestration –> recycling/degradation

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18
Q

desensitization

A

ligand binding promotes phosphorylation of receptor –> beta-arrestin will bind –> now less sensitive to hormones or NTs binding

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19
Q

sequestration

A

after beta-arrestin binds, clathrin-coated vesicles will form –> pulls receptor away from membrane

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20
Q

catecholamines

A

dopamine, norepinephrine, epinephrine

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21
Q

high dose epinephrine

A

increase vasoconstriction, increase inotropy, increase chonotropy, increase HR and BP

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22
Q

low dose epinephrine

A

vasodilation, increase inotropy and chonotropy so still increases HR and CO (increased to overcome vasodilation)

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23
Q

at low doses epinephrine will bind _

A

beta receptors which allows vasodilation

24
Q

at high doses epinephrine binds _

A

alpha receptors which causes vasoconstriction (lower affinity for alpha than beta)

25
Q

epinephrine smooth muscle effects

A

relaxes GI smooth muscle (alpha and beta) and contracts bladder sphincter (alpha only)

26
Q

epinephrine respiratory effects

A

relaxes bronchial smooth muscle

27
Q

epinephrine metabolic effects

A

elevates blood glucose (decreases insulin secretion) and increases metabolism (increases triglyceride lipase activity and FFA)

28
Q

epinephrine therapeutic uses

A

treatment of bronchospasm, relief of hypersensitivity reactions, prolong local anesthetics, topical hemostatic agent

29
Q

low doses of dopamine

A

binds dopamine receptors and causes vasodilation and Na+ reabsorption

30
Q

high doses of dopamine

A

binds beta-1 receptors causing inotropic effects, induces release of NE

31
Q

very high doses of epinephrine

A

binds vascular alpha-1 receptors and causes vasoconstriction

32
Q

life cycle of NTs

A
  1. synthesis
  2. uptake into storage vesicles
  3. release
  4. receptor binding
  5. removal/reuptake
  6. metabolism
33
Q

synthesis of catecholamines

A

tyrosine –> L-DOPA –> dopamine –> norepinephrine or epinephrine

34
Q

rate limiting step in catecholamine synthesis

A

tyrosine hydroxylase hydroxylating tyrosine

35
Q

uptake into storage vesicles

A

dopamine enters a vesicle and is converted to NE or E; protected from degradation in vesicle (presynaptic cell)

36
Q

VMAT1 and VMAT2

A

transport catecholamines into storage vesicles

37
Q

VMAT1

A

peripheral

38
Q

VMAT2

A

CNS

39
Q

reserpine

A

irreversibly binds VMAT and inhibits them from taking up catecholamines; will deplete the storage vesicles

40
Q

therapeutic uses of reserpine

A

antihypertensive; not used because of CNS effects

41
Q

catecholamine release

A

influx of calcium (from AP) causes fusion of the vesicles with the cell membrane through exocytosis

42
Q

catecholamine reuptake

A

norepinephrine transporter (NET) transports back into neuron

43
Q

reuptake inhibiters

A

SNRIs, cocaine, imipramine

44
Q

imipramine

A

tricyclic antidepressant; block NET and prolong stimulation of receptors

45
Q

cocaine

A

blocks NET and DAT; prolongs stimulation of both central and peripheral receptors; can be used as local anesthetic

46
Q

catecholamine metabolism

A

done by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT)

47
Q

MAO-A

A

noradrenergic neurons

48
Q

MAO-B

A

serotonergic and histaminergic neurons

49
Q

COMT

A

not found in sympathetic neurons

50
Q

MAO-A inhibition

A

responsible for antidepressant effects

51
Q

MAO-B inhibition

A

decreases dopamine metabolism in the brain; useful for Parkinson’s

52
Q

safinamide

A

MAO-B inhibitor; Parkinson’s disease

53
Q

isocarboxazid & seleginline

A

MAO inhibitors

54
Q

tolcapone & entacapone

A

COMT inhibitors; Parkinson’s disease (with levodopa)

55
Q

COMT inhibitors

A

inhibit levodopa metabolism, leaving more available for conversion to dopamine

QUIZ 7 (12 decks)

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