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Pharm Exam 1 > Wakade - Adrenergic Pharmacology II > Flashcards

Wakade - Adrenergic Pharmacology II Flashcards

1
Q

Metabolic Degradation of NE and EPI:

By what enzymes?

A

MAO and COMT

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2
Q

MAO:
o Location:
o Action in Nerve Terminals:

A

MAO:
o Location: nerve terminals (mitochondrial outer membrane), brain, liver, intestinal mucosa and neuronal tissue
o Action in Nerve Terminals: metabolizes free NE to regulate transmitter content in cytosol

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3
Q

COMT:

Location

A

Location: effector cells (smooth muscle, cardiac muscle etc.) and liver (cytosol)

Note: NOT found in brain or neuronal cells

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4
Q

Metabolism of NE/EPI:

MAO first
COMT first

A

o MAO first (nerve terminal) followed by COMT (liver)

o COMT first (effector cell or liver) followed by MAO (liver)- primary pathway*

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5
Q

Two Types of Adrenergic Receptors:

A

Alpha

Beta

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6
Q

Alpha Adrenergic Receptors primarily produce:

Exceptions:

A

Alpha: produce primarily CONTRACTION or EXCITATION

Exceptions: inhibition of intestinal smooth muscle, presynaptic nerve terminals, platelets and brain.

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7
Q

Beta Adrenergic Receptors primarily produce:

Exceptions:

A

Beta: produce primarily RELAXATION or INHIBITION

Exceptions: stimulation of heart and kidney cells

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8
Q

Can cell have both alpha and beta R?

Final response depends on what?

A

Cell/organ may have both alpha and beta R: and they may be activated simultaneously

Final response: depends on two factors

  • Dominance of a certain type of receptor
  • Type of adrenergic agent use
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9
Q

Two subtypes of alpha adrenergic R

A

Alpha1: post-synaptic smooth muscles of blood vessels, salivary glands, pancreas, internal sex organs etc.

Alpha2: presynaptic SS nerve terminals, blood platelets, CNS

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10
Q

Potencies:

Phenylphrine (PE) > Methoxamine

A

Alpha1 Phenylphrine (PE) > Methoxamine

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11
Q

Potencies:

Clonidine > Alpha-Methyl-NE&raquo_space; Oxymetazoline

A

Alpha2 Clonidine > Alpha-Methyl-NE&raquo_space; Oxymetazoline

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12
Q

Potencies:

Naphazoline = EPI = NE

A

Alpha1=Alpha2 Naphazoline = EPI = NE

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13
Q

Mechanism of Signaling (Alpha1):

A

Agonist binds Alpha1 receptor (coupled to Gq protein)

Gq alpha subunit released and binds GTP

Gq alpha + GTP –> Activates phospholipase C

PIP2 –> DAG and IP3 (by PLC)

DAG activates PKC

IP3 causes release of stored Ca++ and increase in free Ca++ (activates protein kinases)

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14
Q

Mechanism of Signaling (Alpha2):

A

Agonist binds Alpha2 receptor (coupled to Gi protein)

GTP kicks off GDP and binds Gi alpha subunit

Gi alpha + GTP –> Inhibits adenylyl cyclase –> decrease in cAMP

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15
Q

Beta-Adrenergic Receptors:
Two Subtypes:
Locations:

A

Beta1: located in the heart, kidney and adipose cells

Beta2: located in the vascular and bronchial smooth muscles

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16
Q

Potency

Beta 1

A

ISO > EPI > NE&raquo_space;> PE

17
Q

Potency

Beta2

A

ISO > EPI&raquo_space;> NE&raquo_space;> PE

18
Q

Mechanism of Signaling (beta adrenergic receptors)

A

Agonist binds Beta receptor (coupled to Gs protein)

GTP kicks off GDP and binds to Gs alpha subunit

Gs alpha + GTP –> Activates adenylyl cyclase (AC) –> Increase in cAMP

Increase in cAMP –> Activation of various proteins and enzymes

19
Q

Dopamine Receptors:
Location of major effects
What type of drugs act on DA receptors?

A

Major Effects: in CNS

Antipsychotics and neuroleptic drugs act through DA receptors

20
Q

Two subtypes of DA-Rs

A

D1 and D2

21
Q

D1 Family:

Subtype:
Effect:
Location:
Effects on smooth muscle cells of BVs
What is particularly rich in D1 receptors?
A

D1 Family (D5 Subtype):

Effect: increases cAMP

Location: Mainly CNS (striatum, hypothalamus, hippocampus)
Also in smooth muscle cells of blood vessels (particularly in renal vasculature)

  • Vasodilation
  • Natriuresis (loss of Na+)
  • Diuresis

Renal vasculature

22
Q

D2 Family:

Subtype:
Effect:
Location: (3)

Stimulation effects: (3)

A

(D3,D4 Subtypes):

Inhibits cAMP, blocks Ca++ channels and opens K+ channels

Location:
o Sympathetic ganglia
o Sympathetic nerve terminals
o Abundant in CNS (pituitary gland, substantia nigra, frontal cortex, medulla, hypothalamus)

Stimulation Effects:
o Hypotension
o Bradycardia
o Vasodilation

23
Q

Relative Dopamine Potencies:

A

Dopamine: D1 = D2&raquo_space; beta&raquo_space; alpha

Fenoldopam: D1&raquo_space; D2

24
Q

Production of CV Actions by 3 Mechanisms:

A
  1. Releasing NE from adrenergic neurons (indirectly acting sympathomimetic)
  2. Interacting with alpha and beta adrenergic receptors
  3. Interacting with specific DA receptors
25
Q

What do high doses of DA produce?

Due to:

A

Cause increased HR, increased contraction and increased CO

Due to activation of beta receptors by NE released from SS neurons in the heart

26
Q

Adrenergic responses of organs:

Heart:

A

Heart: beta1 receptors mediate all actions

27
Q

Adrenergic responses of organs:

Effect on heart rate:

A

o Rate: INCREASED

Activation of beta1 R in pacemaker cells of SA node –> more rapid diastolic depolarization and an increase in the frequency of APs

Important point: if the amine causes a rise in BP (ie. NE or PE), reflex activation of the vagus may override the direct action on the heart –> SLOWING of heart rate

28
Q

What causes more rapid diastolic depolarization/increase in frequency of AP?

A

NE accelerates the process of decreasing K+ permeability during diastolic interval
- Results in cell being able to reach threshold faster and fire APs faster

29
Q

Adrenergic responses of heart:
Contractile force:

Effect of activation of beta1-R on myocardial cells:

Affect of Ca influx on the AP:

A

o Contractile Force: INCREASED

Activation of beta1 R of myocardial cells INCREASES Ca++ influx with each AP –> greater force of contraction

Increase in Ca++ influx occurs with LITTLE (IF ANY) CHANGE to the AP itself

30
Q

Adrenergic responses of heart:
Contractile force:

Conduction: INCREASED

A

Velocity of impulse transfer from SA and AV nodes is increased

Refractory period of AV node is decreased

31
Q

Adrenergic responses of heart:
Arrhythmias:

Can be induced by:

More common with NE, EPI, or ISO?

What enhances the effects of NE?

A

o Arrhythmias:

Can be induced by activation of beta1 R

Concomitant rise in BP will also increase the possibility (ie. due to increased workload on the heart)

Therefore, arrhythmias are more common with NE and EPI than with ISO

Some general anesthetics (ie. halothane) enhance these effects of NE

32
Q

Adrenergic responses of heart:

Cardiac efficiency:

A

o Cardiac Efficiency: DECREASED*

CE= Work/O2 Used
- Work=↑↑
- O2=↑↑↑
Therefore, although both work and O2 increase, the O2 used is increased higher to accommodate the increased work, resulting in an overall decrease in CE

Pharm Exam 1 (23 decks)

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