Neuropharmacology: Agents That Act On Adrenergic Nerve Terminals

Front 1

Name 4 categories of agents that act on presynaptic nerve terminal

Back 1

1. Drugs that interfere with storage and/or release of the transmitter
2. DOPA drugs
3. Drugs that block neurotransmitter reuptake
4. Drugs that inhibit metabolism (MAOI's & COMTI's)

Front 2

Effects of inhibitiors of transmitter storage and/or release are prevented by (blank).

Back 2

reuptake blockers

(cocaine, antidepressants)

Front 3

Chronic use of inhibitors of transmitter release/storage could lead to what?

Back 3

supersensitivity to direct acting agonists.

The inhibitors of transmitter release/storage prevent transmitter from getting into synapse, thus the postsynaptic receptors are upregulated.

Front 4

Reserpine mechanism

Back 4

inhibits synaptic vesicle uptake pump, leading to depletion of monoamine transmitters

Front 5

Guanethidine mechanism

Back 5

accumulates in synaptic vesicle & causes slow release & depletion of NE

Front 6

Bretylium mechanism

Back 6

inhibits NE release

Front 7

Reserpine
Bretylium
Guanethidine

Which is active in CNS?
Which does not affect vesicle stores?

Back 7

Reserpine acts in CNS.

Bretylium does not affect vesicle stores

Front 8

Guanethidine, Bretylium, Reserpine are mainly indicated for what?

Back 8

treatment of hypertension

Front 9

Toxic effects of Reserpine

Back 9

sedation
nightmares
severe depression

Front 10

Levodopa mechanism

Back 10

1. gets into CNS
2. converted to DA
3. more DA released in CNS terminals

Front 11

Carbidopa mechanism

Back 11

inhibits DOPA decarboxylase in the PNS so that Levodopa is not converted to DA before it reaches the CNS

Front 12

Methyldopa mechanism

Back 12

1. into CNS
2. converted to alpha-methyl NE
3. alpha-methyl NE is alpha-2 agonist
4. causes decrease in BP

Front 13

Difference between Clonidine and Methyldopa

Back 13

Clonidine = direct alpha-2 agonist

Methyldopa = indirect alpha-2 agonist

Front 14

Reuptake blockers mechanism

Back 14

block reuptake of monoamine transmitters, thereby increasing concentration of those monoamine transmitters in the synapse

Front 15

2 examples of reuptake blockers

Back 15

cocaine
antidepressants

Front 16

Cocain produces a pronounced increase in this neurotransmitter in the brain, leading to euphoria

Back 16

dopamine

Front 17

Selegiline

Back 17

MAOI

Front 18

Reserpine

Back 18

inhibitor of transmitter storage/release

Front 19

Guanethidine

Back 19

inhibitor of transmitter storage/release

Front 20

Betrylium

Back 20

inhibitor of transmitter release

Front 21

Antidepressants

Back 21

reuptake blockers

Front 22

Describe paradoxical effect of MAOI's on blood pressure

Back 22

1. MAO inhbition leads to increased levels of tyramine
2. tyramine gets into nerve terminal
3. tyramine converted to octopamine by dopamine-beta-hydroxylase
4. octopamine is a false transmitter & has no efficacy
5. sympatholytic effect due to decreased NE
6. end result = lowered BP

Front 23

Effect of MAOI's on indirect adrenergic agonists

Back 23

MAOI's potentiate indirect agonist action

Front 24

What happens when a person is on an MAOI and has too much tyramine in their diet?

Back 24

1. Tyramine overwhelsm dopamine-beta-hydroxylase
2. octopamine not produced
3. instead, lots of NE produced
4. more NE = increase in BP, HR, CO

Front 25

Clinical uses of MAOI's

Back 25

1. adjunct to levodopa/carbidopa treatment
2. antidepressants

Front 26

Entacapone

Back 26

COMT inhibitor

Front 27

Patients taking COMT inhibitors will have exaggerated effects if given these.

Back 27

catecholamines

(dopamine, epinephrine)