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PT 1 > L13, 14, 15 Adrenergic Receptor Agonists and Antagonists > Flashcards

L13, 14, 15 Adrenergic Receptor Agonists and Antagonists Flashcards

1
Q

The sympathetic system is the ___ division of the ANS; the parasympathetic system is the ___ division of the ANS.

A

Thoracolumbar; craniosacral

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2
Q

The sympathetic system has ___ arms, ___ fingers the parasymapthetic system has ___ arms, ___ fingers.

A

Short; long

Long; short

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3
Q

Describe the exception of the adrenal gland.

A

Pre-ganglionic fibers project to the adrenal gland; ACh is released, which activates chromathin cells to produce NE/E. The hormones are released directly into circulation. There is no post-ganglionic nerve fiber

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4
Q

Pre-ganglionic fibers release ___.

A

ACh

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5
Q

Post-ganglionic parasympathetic fibers release ___.

A

ACh

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6
Q

Post-ganglionic sympathetic fibers release ___. What is the exception to this?

A

NE; sympathetic fibers innervating sweat glands and some skeletal muscle blood vessels release ACh

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7
Q

The adrenal gland releases ___ and ___.

A

NE and EPI

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8
Q

True or false - some organs receive dual ANS innervation and some do not.

A

True

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9
Q

Describe the effects of the parasympathetic system on the following organs: eye, heart, bronchioles, GI tract, bladder

A

Eye: pupillary constriction (miosis), accommodation
Heart: negative chronotropy (bradycardia)
Bronchioles: constriction of smooth muscle
GI tract: increased motility, secretions
Bladder: stimulates emptying

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10
Q

Describe the effects of the sympathetic system on the following organs/functions: eye, heart, bronchioles, blood vessels, GI tract, bladder, metabolic functions

A

Eye: pupillary dilation (mydriasis)
Heart: increased chronotropy and inotropy
Bronchioles: smooth muscle relaxation
Blood vessels: constriction or relaxation
GI: decreased motility
Bladder: inhibits emptying
Metabolic functions: increased blood sugar

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11
Q

Parasympathetic innervation of the eye leads to constriction of the ___, causing miosis, and constriction of the ___, leading to accommodation.

A

Sphincter muscles of the pupil; ciliary muscles

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12
Q

Parasympathetic innervation of the heart reduces heart rate via the ___ and reduces conduction via the ___.

A

SA node; AV node

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13
Q

Parasympathetic innervation of the bladder leads to contraction of the ___, causing bladder emptying.

A

Detrusor muscle

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14
Q

Sympathetic innervation of the eye leads to constriction of the ___, causing mydriasis, and activation of the ___, leading to production of aqueous humor.

A

Dilator muscle; ciliary epithelium

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15
Q

Sympathetic innervation of the heart increases heart rate via what process?

A

Accelerated SA node pacemaker depolarization

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16
Q

What are the three main currents that contribute to SA node membrane potential?

A
  1. Inward calcium current
  2. Funny current
  3. Outward potassium current
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17
Q

How does sympathetic innervation accelerate SA node pacemaker depolarization?

A

Increases inward calcium current and funny current to promote faster phase 4 depolarization and lower the threshold for activation; it also stimulates increased calcium influx into myocytes, leading to greater contractile force

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18
Q

Upon what two variables does the outcome of sympathetic innervation of blood vessels depend?

A
  1. Relative density of receptor population (alpha1 vs. beta2) in the targeted vascular bed
  2. Ligand available to mediate the vascular response (NE vs. E)
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19
Q

Sympathetic innervation of the bladder leads to contraction of the ___ and relaxation of the ___, leading to inhibition of emptying.

A

Urethral sphincters; detrusor muscle

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20
Q

What are the 5 broad steps of adrenergic neurotransmission?

A
  1. Synthesis
  2. Storage in vesicles
  3. Release of catecholamines
  4. Binding of NT to post- or pre-synaptic sites
  5. Termination of action
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21
Q

What happens during synthesis of adrenergic NT?

A

Tyrosine hydroxylase (rate-limiting enzyme) converts tyrosine to DOPA. DOPA is metabolized to DA. Half of DA is transported into vesicles via VMAT (the other half is metabolized)

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22
Q

What happens during vesicle storage of adrenergic NT?

A

Dopamine can be converted to NE via dopamine beta-hydroxylase. EPI can be produced from NE via phenylethanolamine-N-methyltransferase. EPI and NE are also produced in the adrenal medulla.

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23
Q

What happens during release of catecholamines?

A

Voltage dependent opening of calcium channels elevates intracellular calcium and stimulates the interaction of SNARE proteins to enable vesicle fusion and exocytosis of the vesicle contents

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24
Q

The action of a NT depends upon what three things?

A
  1. Receptor type
  2. Second messenger system
  3. Machinery of the cell type
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25
Q

What are the three mechanisms of termination of action?

A
  1. Re-uptake into nerve terminals or post-synaptic cell
  2. Diffusion out of synaptic cleft
  3. Metabolic transformation
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26
Q

Where are alpha1 receptors located?

A
  1. Most vascular smooth muscle*
  2. Pupillary dilator muscle*
  3. Pilomotor smooth muscle
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27
Q

Where are alpha2 receptors located?

A
  1. Adrenergic and cholinergic nerve terminals*
  2. Platelets
  3. Some vascular smooth muscle
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28
Q

Where are beta1 receptors located?

A
  1. Heart*

2. Juxtaglomerular cells*

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29
Q

Where are beta2 receptors located?

A
  1. Respiratory, uterine, and vascular smooth muscle*
  2. Liver*
  3. Pancreatic beta cells
  4. Somatic motor nerve terminals (voluntary muscle)*
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30
Q

Where are beta3 receptors located?

A
  1. Fat cells
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31
Q

Where are dopamine1 receptors located?

A
  1. Renal and other splanchnic blood vessels*
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32
Q

Where are dopamine2 receptors located?

A

1.Nerve terminals

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33
Q

What are the effects of binding alpha1 receptors?

A
  1. Contraction of vascular smooth muscle*
  2. Contraction of pupillary dilator muscle (mydriasis)*
  3. Contraction of pilomotor smooth muscle (erects hair)
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34
Q

What are the effects of binding alpha2 receptors?

A
  1. Inhibition of NT release at adrenergic and cholinergic nerve terminals*
  2. Stimulates aggregation of platelets
  3. Contracts some vascular smooth muscle
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35
Q

What are the effects of binding beta1 receptors?

A
  1. Stimulates increased rate and force of heart*

2. Stimulates renin release from juxtaglomerular cells*

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36
Q

What are the effects of binding beta2 receptors?

A
  1. Relaxation of respiratory, uterine, and vascular smooth muscle*
  2. Stimulates glycogenolysis in the liver*
  3. Stimulates insulin release from pancreatic beta cells
  4. Causes a tremor via somatic motor nerve terminals*
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37
Q

What are the effects of binding beta3 receptors?

A
  1. Stimulates lipolysis in fat cells
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38
Q

What are the effects of binding dopamine1 receptors?

A
  1. Relaxes (reduces resistance) renal and other splanchnic blood vessels*
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39
Q

What are the effects of binding dopamine2 receptors?

A
  1. Inhibits adenylyl cyclase at nerve terminals
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40
Q

Alpha1 adrenergic receptors are positively coupled to ___ via which G-protein?

A

PLC; G-alpha-q

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41
Q

Describe what happens in vascular smooth muscle when an agonist binds to an alpha1 adrenergic receptor.

A
  1. Agonist binds receptor
  2. G-alpha-q subunit activates PLC
  3. PLC liberates IP3 and DAG
  4. IP3 activates an IP3 receptor that acts as a calcium release channel in the SR
  5. Calcium is released into the intracellular space, increasing [Ca2] and stimulating smooth muscle contraction
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42
Q

Alpha2 adrenergic receptors are negatively coupled to ___ via which G-protein?

A

Adenylyl cyclase; G-alpha-i subunit

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43
Q

Describe what happens at an adrenergic nerve terminal when an agonist binds to an alpha2 adrenergic receptor.

A
  1. Agonist binds to alpha-2 receptor
  2. G-alpha-i inhibits adenylyl cyclase
  3. This reduces cAMP, which reduces activation of PKA
  4. Phosphorylation of N-type calcium channels on nerve terminals is reduced, reducing calcium influx during membrane depolarization and reducing vesicular release of NT
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44
Q

Beta1 adrenergic receptors are positively coupled to ___ via which G-protein?

A

Adenylyl cyclase; G-alpha-s

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45
Q

Describe what happens in a cardiac pacemaker cell when an agonist binds to an beta1 adrenergic receptor.

A
  1. Agonist binds beta1 receptor
  2. G-alpha-s activates adenylyl cyclase
  3. Adenylyl cyclase produces cAMP
  4. cAMP activates PKA
  5. PKA phosphorylates Ca2+ channels in the membrane of SA node cells, leading to increased slow inward calcium current and faster nodal cell depolarization
  6. cAMP also directly activates funny currents to increase the slope of depolarization
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46
Q

Describe what happens in a cardiac myocyte cell when an agonist binds to an beta1 adrenergic receptor.

A
  1. Agonist binds beta1 receptor
  2. G-alpha-s activates adenylyl cyclase
  3. Adenylyl cyclase produces cAMP
  4. cAMP activates PKA
  5. PKA phosphorylates L-type calcium channels in myocyte membranes, leading to enhanced calcium influx and larger trigger signals for release of Ca2+ from the SR. Trigger calcium also enters the SR, increasing storage so that the next trigger initiates larger efflux of calcium.
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47
Q

Beta2 adrenergic receptors are positively coupled to ___ via which G-protein?

A

Adenylyl cyclase; G-alpha-s

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48
Q

Describe what happens in vascular smooth muscle when an agonist binds to an beta2 adrenergic receptor.

A
  1. Agonist binds beta1 receptor
  2. G-alpha-s activates adenylyl cyclase
  3. Adenylyl cyclase produces cAMP
  4. cAMP activates PKA
  5. PKA phosphorylates and INHIBITS MLCK. This prevents actin and myosin from interacting/muscle from contracting. This phosphorylation also reduces the affinity of MLCK for Ca-calmodulin, resulting in further reduction.
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49
Q

Describe what happens in vascular smooth muscle when an agonist binds to an alpha2 adrenergic receptor.

A

Peripheral vasoconstriction through the opposite mechanism of beta-adrenergic receptors.

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50
Q

What are the two categories of adrenomimetic agnoists?

A
  1. Direct-acting

2. Indirect-acting

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51
Q

What are the 2 categories of indirect-acting adrenomimetic agonists?

A
  1. Releasers

2. Reuptake inhibitors

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52
Q

What are the 2 categories of direct-acting adrenomimetic agonists?

A
  1. Alpha agonists

2. Beta agonists

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53
Q

What are the 3 categories of alpha agonists?

A
  1. Nonselective
  2. Alpha-1 selective
  3. Alpha-2 selective
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54
Q

What are the 3 categories of beta agonists?

A
  1. Nonselective
  2. Beta-1 selective
  3. Beta-2 selective
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55
Q

What are the 3 endogenous ligands for adrenergic receptors?

A

NE, EPI, DA

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56
Q 
MAP = ?
CO = ?
A

CO*TPR

HR * SV

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57
Q

Total peripheral resistance (TPR) has a predominant effect on ___.

A

Diastolic pressure (determines rate at which blood leaves the arteries through the resistance vessels)

58
Q

Cardiac output (CO) has a predominant effect on ___.

A

Systolic pressure (contractility of the heart forces SV into the arterial tree during systole)

59
Q

TPR and diastolic pressure are affected more by ___ receptors expressed in the ___.

A

Alpha1, alpha2, and beta-2 adrenergic; vasculature

60
Q

CO and systolic pressure are affected more by ___ receptors expressed in ___.

A

Beta1 adrenergic; cardiac tissue

61
Q

What are the physiologic effects of epinephrine?

A
  1. Low dose: lower diastolic blood pressure (beta2), increase CO/systolic BP (beta1)
  2. Higher dose: increase TPR and CO (alpha1, alpha2, beta1)
  3. Bronchodilation (beta2)
  4. Decreased bronchial secretions (alpha1)
62
Q

What are the potential toxicities of epinephrine?

A
  1. Arrhythmias*
  2. Cerebral hemorrhage
  3. Anxiety
  4. Cold extremities
  5. Pulmonary edema
63
Q

What adrenergic receptors does epinephrine stimulate?

A

Alpha1, Alpha2, Beta1, Beta2 (beta predominates at lower concentrations)

64
Q

What are the indications of epinephrine?

A
  1. Anaphylaxis*
  2. Cardiac arrest*
  3. Bronchospasm*
65
Q

What are the contraindications of epinpherine?

A

Later term pregnancy

66
Q

Why is epinephrine short-acting?

A

It is very susceptible to degradation

67
Q

What receptors doe NE stimulate?

A

Alpha1, alpha2, beta1

68
Q

What are the physiological effects of NE?

A
  1. Increase CO/HR/systolic BP (beta1)
  2. Increase TPR/diastolic BP (alpha1, alpha2)
  3. Decrease HR (baroreflex)
  4. Overall increase in MAP
69
Q

What are the toxicities of NE?

A
  1. Arrhythmias
  2. Ischemia*
  3. Hypertension
70
Q

What are the indications of NE?

A
  1. Vasodilatory shock*
71
Q

What are the contraindications of NE?

A
  1. Pre-existing vasoconstriction or ischemia*

2. Late term pregnancy

72
Q

NE is susceptible to degradation by metabolic enzymes; thus, it has a short ___ and must be given by controlled ___.

A

Half-life; infusion

73
Q

What receptors does DA stimulate?

A

Dopamine1, dopamine2, beta1, alpha1, alpha2

74
Q

What are the physiological effects of DA?

A
  1. At low rate: decrease TPR (dopamine1) and increase CO (beta1)
  2. At high rate: increase MAP and TPR (alpha1, alpha2, beta1)
75
Q

What are the toxicities of DA?

A
  1. Low BP (low infusion rates)*

2. Ischemia (high infusion rate)*

76
Q

What are the indications of DA?

A
  1. Cardiogenic shock*
77
Q

What are the contraindications of DA?

A
  1. Tachyarrhythmias*

2. V. fib.

78
Q

What is isoproterenol?

A

Non-selective beta-adrenergic agonist (no affinity for alpha receptors)

79
Q

What receptors does isoproterenol stimulate?

A

Beta1, beta2

80
Q

What are the physiological effects of isoproterenol?

A
  1. Decrease TPR, decrease diastolic BP (beta2)
  2. Increase CO, increase systolic BP transiently, but this is overcome by #1 (beta1)
  3. Small decrease in MAP
  4. Bronchodilation (beta2)
81
Q

What are the toxicities of isoproterenol?

A
  1. Tachyarrhythmias*
82
Q

What are the indications of isoproterenol?

A
  1. Bradycardia w/heart block when TPR is high
83
Q

What are the contraindications of isoproterenol?

A
  1. Angina w/arrhythmias
84
Q

What is dobutamine?

A

Selective beta-1 adrenergic receptor agonist

85
Q

What does dobutamine bind to?

A

Beta1>beta2>alpha (considered selective for beta1)

86
Q

What are the physiological effects of dobutamine?

A
  1. Increase CO (beta1)
    * Note that the inotropic effect is > than the chronotropic effect due to lack of beta-2 mediated vasodilation and reflex tachycardia
87
Q

What are the toxicities of dobutamine?

A
  1. Arrhythmias (beta1)
  2. Hypotension (beta2)*
  3. Hypertension (beta1)
88
Q

What are the indications of dobutamine?

A
  1. Short-term fix for CHF or cardiogenic shock*

2. Excess beta-blockade*

89
Q

What are terbutaline and albuterol?

A

Selective beta-2 adrenergic agonists

90
Q

What are the physiological effects of terbutaline and albuterol

A
  1. Bronchodilation
  2. Uterine relaxation
  3. Negligible cardiovascular effects (can cause some beta agonist-like responses)
91
Q

What are the toxicities of terbutaline and albuterol?

A
  1. Tachycardia (beta1)*
  2. Muscle tremor (beta2)*
  3. Tolerance (beta2)*
92
Q

What are the indications of terbutaline and albuterol?

A
  1. Bronchospasm*

2. Chronic treatment of obstructive airway disease*

93
Q

What is phenylephrine?

A

Selective alpha1 adrenergic receptor agonist

94
Q

Phenylephrine is not a catecholamine; why is this important?

A

It is not subject to COMT degradation.

95
Q

What are the physiological effects of phenylephrine?

A
  1. Increase TPR and MAP
  2. Decrease HR (baroreflex)
  3. Pupillary dilation
  4. Decrease bronchiole and sinus secretions
96
Q

What are the toxicities of phenylephrine?

A
  1. Hypertension*
97
Q

What are the indications of phenylephrine?

A
  1. Hypotension during anesthesia
  2. SV tachycardia*
  3. Mydriatic agent in ophthalmic issues*
  4. Nasal congestion*
98
Q

What are the contraindications of phenylephrine?

A
  1. Hypertension

2. V. tach.

99
Q

What is clonidine?

A

Selective alpha2 adrenergic receptor agonist

100
Q

What are the physiological effects of clonidine?

A
  1. Acute increase in BP (peripheral effect)

2. Reduced BP (central effect by crossing BBB)

101
Q

What are the toxicities of clonidine?

A
  1. Dry mouth*
  2. Sedation
  3. Bradycardia
  4. Hypertensive crisis after acute withdrawal*
102
Q

What are the indications of clonidine?

A
  1. Hypertension due to sympathetic activation*
103
Q

What are indirect acting sympathomimetics?

A

Drugs that increase [endogenously released catecholamines] at site of release

104
Q

Upon what do the effects of indirect acting sympathomimetics depend?

A

Whether the drug can cross the BBB

105
Q

What are the 6 major indirect acting sympathomimetics (releasing agents)?

A
  1. Amphetamine
  2. Methamphetamine
  3. Methylphenidate
  4. Ephedrine
  5. Pseudoephedrine
  6. Tyramine
106
Q

What are the physiological effects of the indirect acting sympathomimetics (releasing agents)?

A
  1. Increased TPR and diastolic BP (alpha1, alpha2)
  2. Positive inotropic/chronotropic effects, increased systolic BP (beta1)
  3. CNS stimulant (increased NE)
  4. Anorexia (increased DA)
107
Q

What are the toxicities of the indirect acting sympathomimetics (releasing agents)?

A
  1. Tachycardia (beta1)*

2. Anxiety (?)

108
Q

What are the indications of the indirect acting sympathomimetics (releasing agents)?

A
  1. ADD*
  2. Narcolepsy*
  3. Nasal congestion*
109
Q

What are the contraindications of the indirect acting sympathomimetics (releasing agents)?

A
  1. Hypertension
  2. Severe atherosclerosis
  3. History of drug abuse
  4. Treatment with MAO inhibitors within 2 weeks*
110
Q

What are the three main categories of beta-blockers?

A
  1. Non-selective (beta1, beta2)
  2. Cardioselective (beta1)
  3. Partial agonist (beta1, beta2)
111
Q

What are the three classic non-selective beta-blockers?

A
  1. Propranolol
  2. Timolol
  3. Nadolol
112
Q

What are the two classic cardioselective beta blockers (plus 1 new one)?

A
  1. Atenolol
  2. Metoprolol
  3. Esmolol (new)
113
Q

What is the one classic partial agonist beta blocker?

A

Pindolol

114
Q

Compare the effects of the three categories of beta-blockers on heart rate and force of contraction.

A

All 3 decrease the rate and force of contraction; however, the partial agonist has a limited bradycardic response due to the partial agonist activity

115
Q

Compare the effects of the three categories of beta-blockers on peripheral resistance.

A
  1. Non-selective: increased, due to unopposed vasoconstriction by alpha1-receptors
  2. Cardioselective: little effect, as beta-receptors are not blocked
  3. Partial agonist: slight decrease because of partial beta2 agonist properties
116
Q

Compare the effects of the three categories of beta-blockers on renin release.

A

All three decrease release of renin

117
Q

Compare the effects of the three categories of beta-blockers on the bronchioles.

A
  1. Non-selective: bronchoconstriction, particularly in asthmatics
  2. Cardioselective: Less bronchoconstriction, but still not recommended in asthmatics
  3. Ditto
118
Q

Compare the effects of the three categories of beta-blockers on glucose metabolism.

A
  1. Non-selective: inhibits effects of EPI; use caution with diabetics using insulin, as it masks symptoms of hypoglycemia
  2. Little effect
  3. Reduced response to EPI because of partial agonist, but still not as potent as endogenously-released EPI
119
Q

What are the physiological effects of the non-selective beta-blockers?

A
  1. Decreased HR
  2. Decreased contractility
  3. Decreased renin release
  4. Reduced sympathetic activation
  5. Inhibition of aqueous humor producttion
120
Q

What are the toxicities of the non-selective beta-blockers?

A
  1. Bronchospasm*
  2. Mask symptoms of hypoglycemia*
  3. Insomnia
  4. Depression
  5. Bradycardia*
  6. Increased triglycerides*
121
Q

What are the indications of the non-selective beta-blockers?

A
  1. Hypertension*
  2. Angina*
  3. Glaucoma*
  4. Early to moderate heart failure*
  5. Arrhythmia*
  6. Thyrotoxicosis
  7. Anxiety
122
Q

What are the contraindications of the non-selective beta-blockers?

A
  1. Bronchospasm during asthma*
  2. Sinus bradycardia*
  3. 2nd and 3rd degree heart block*
  4. Cardiogenic shock*
123
Q

What are the physiological effects of the cardioselective beta-blockers?

A
  1. Decreased HR
  2. Decreased contractility
  3. Decreased renin release
  4. Reduced sympathetic activation
124
Q

What are the toxicities of the cardioselective beta-blockers?

A
  1. Dizziness
  2. Depression
  3. Insomnia
  4. Hypotension*
  5. Bradycardia*
125
Q

What are the indications of the cardioselective beta-blockers?

A
  1. Hypertension*
  2. Angina*
  3. Arrhythmia*
126
Q

What are the contraindications of the cardioselective beta-blockers?

A
  1. Sinus bradycardia*
  2. 2nd and 3rd degree heart block*
  3. Cardiogenic shock*
127
Q

When is it beneficial to use a partial agonist beta blocker?

A

When symapthetic activity is high

128
Q

What are the physiological effects of the partial agonist beta-blockers?

A
  1. Decreased BP
  2. Decreased contractility
  3. Decreased renin release
  4. Reduced sympathetic activation
129
Q

What are the toxicities of the partial agonist beta-blockers?

A
  1. Dizziness
  2. Depression
  3. Insomnia
  4. Hypotension*
130
Q

What are the indications of the partial agonist beta-blockers?

A
  1. Hypertension when other beta blockers are less well-tolerated*
131
Q

What are the contraindications of the partial agonist beta-blockers?

A
  1. Sinus bradycardia*
  2. 2nd and 3rd degree heart block*
  3. Cardiogenic shock*
132
Q

What are the two classic non-selective alpha-receptor antagonists (classify as reversible/irreversible)?

A
  1. Phenoxybenzamine (irreversible)

2. Phentolamine (reversible)

133
Q

What are the physiological effects of the non-selective alpha-blockers?

A
  1. Decreased BP (alpha blockade unmasks beta effect)

2. Increased inotropy and chronotropy

134
Q

What are the toxicities of the non-selective alpha-blockers?

A
  1. Prolonged hypotension*
  2. Reflex tachycardia*
  3. Nasal congestion
135
Q

What are the indications of the non-selective alpha-blockers?

A
  1. Hypertension associated w/pheochromocytoma*

2. Vasoconstrictor-induced extravasation*

136
Q

What are the contraindications of the non-selective alpha-blockers?

A
  1. Coronary artery disease
137
Q

What are the selective alpha1 adrenergic blockers?

A
  1. Prazosin
  2. Doxazosin
  3. Terazosin
138
Q

What are the physiological effects of the alpha1 adrenergic blockers?

A
  1. Inhibits vasoconstriction

2. Prostate smooth muscle relaxation

139
Q

What are the toxicities of the alpha1 adrenergic blockers?

A
  1. Syncopy

2. Orthostatic hypotension*

140
Q

What are the indications of the alpha1 adrenergic blockers?

A
  1. Hypertension*

2. Bengin prostatic hyperplasia (BPH)*

PT 1 (34 decks)

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