Pharm Adrenergic

Front 1

These G-proteins are activated by which receptors?
Gi
Gs
Gq

Back 1

Gi - alpha2
Gs - beta1 beta 2
Gq - alpha1

Front 2

Mechanism:

Guanethidine

Back 2

Guanethidine enters the NET, uncouples AP from calcium entry, and stabilizes the vesicular membrane.

Front 3

Mechanism:

Reserpine

Back 3

Reserpie enters the terminal, stabilizes the vesicular membrane, causing depletion of NE over time.

It keeps NE from being stored.

Front 4

You are NE.
What receptor do you like?

Back 4

Alpha1 +4
Beta1 +4

Front 5

You are Isoproterenol.
What receptor do you like?

Back 5

Beta1
Beta2

Front 6

You are Epi (low)
What receptor do you like?

Back 6

Beta1 +3
Beta2 +3

Front 7

You are Epi (high)
What receptor do you like!

Back 7

Alpha1 +4
Beta1 +4
Beta2 +4

Front 8

You are Dopamine (low)
What receptor do you like?

Back 8

DA +2
Beta1 +2
Beta2 +1

Front 9

You are Dopamine (high)
What receptor do you like?

Back 9

Alpha1, Beta1, Beta2, DA +4
(equally)

Front 10

You are Dobutamine (low)
What receptor do you like?

Back 10

Beta1

Front 11

You are Dobutamine (high)
What receptor do you like?

Back 11

Beta1 +4
Alpha1, Beta2 +2

*Loses selectivity at higher doses
*Low dose is Beta1 >> Beta2

Front 12

Beta1's favorite agonist

Back 12

Isoproterenol > epi = norepi

Front 13

Alpha1's favorite agonist?

Back 13

Epi > NE >> iso

Front 14

Beta2's favorite agonist?

Back 14

iso > epi >> NE

Front 15

Describe the synthesis of NE:

Back 15

Tyrosine > into the neuron actively > Dopa > Dopamine > into vesicle actively > Dopamine-Beta-Hydroxylase makes NE

Front 16

What's the interaction of tyramine when using an MAOI?

Back 16

Can cause hypertensive crisis (MAO is the gut normally metabolizes tyramine, but with a MAO-i this is reduced, tyramine becomes Octopamine in the neuron which then enters the vesicle, displacing the NE. With no MAO to metabolize it, the excess NE reverses the NET and dumps the NE into the synapse, causing hypertensive crisis)

Front 17

What is unique about Dobutamine?

Back 17

It increases contractility WITHOUT increasing heart rate, via beta-1 stimulation.

Front 18

What are the 4 rules of catecholamines?

Back 18

1: Increasing size of amino group substitution increases beta receptor affinity.
2: -OH groups at 3 & 4 positions confer maximum alpha and beta activity.
3: Removal of -OH from ring increases CNS penetration.
4: Non catecholamines are not metabolized by COMT; substitution of the alpha-Carbon blocks MAO metabolism. (amphetamine has a longer half-life)

Front 19

Structurally, beta agonists have what feature?

Back 19

Beta agonists have greater amino group substitution.
Dobutamine

Front 20

Structurally, what increases the likelihood for CNS penetration?

Back 20

Lack of -OH group on the ring helps it to get into the CNS, but it will have less affinity/activity at Alpha and Beta receptors.

Front 21

What determines how catecholamines and non-catecholamines are metabolized?

Back 21

Non-catecholamines are not metabolized by COMT.

Substitution of the Alpha-Carbon blocks MAO metabolism.

Front 22

How is blood pressure affected by Dopamine?

Back 22

BP decreased by DA receptors in renal and mesenteric beds where perfusion is increased.

BP decreased by Beta2 activation.

BP increased (very high dose) by Alpha1 activation.

Front 23

Phenylephrine is an example of what?

Back 23

Non-catecholamine (not metabolized by COMT)

Alpha1 stimulant

Front 24

Ephedrine is an example of what?

Back 24

Weak Alpha-1 and Beta agonist.

It also enhances the release of NE.

A CNS stimulant.

Nasal decongestant and pressor agent.

Front 25

How do Xanthines work?

Back 25

Inhibit phosphodiesterase, to stop the breakdown of cAMP. Gives the same effect as beta stimulation, because cAMP increases.

Aslo, they antagonize adenosine receptors causing CNS stimulating effects. It knocks adenosine off the "sleepy receptors".

Front 26

Is reflex tach worse with selective or non-selective alpha blockers?

Back 26

Reflex tach is WORSE with non-selective alpha blockers than with a selective alpha-1 blocker, because if alpha-2 is blocked there is no feedback inhibition. More NE is released, causing more Beta-1 stimulation and faster HR.

Phentolamine is non-selective.
Decrease BP
Increase HR (reflex)

Front 27

Draw what Epi reversal looks like in Dog-Lab. Which alpha blocker are they likely to use?

Back 27

Phentolamine (non-selective alpha blocker)

Front 28

What are the vascular and blood pressure effects of non-selective Beta-blockers?

Back 28

1: Reduction in Cardiac Output (more pronounced during exercise)

2: Reduction in plasma renin

3: Decrease in sympathetic tone via effects in CNS

B2 block may increase TPR slightly. Decrease in renin due to B1 block. NET EFFECT: reduction in BP.

Decreased conduction velocity, O2 demand and rate of depolarization.

Front 29

Which agonists are used in pregnancy for essential hypertension?

Back 29

alpha-methyl-dopa