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Pharmacology > Autonomic Neurotransmission - Adrenergic transmission > Flashcards

Autonomic Neurotransmission - Adrenergic transmission Flashcards

1
Q

What are the steps involved in adrenergic transmission?

A

◦ Norepinephrine (NE) synthesis:
◦ Tyrosine → DOPA → Dopamine → Norepinephrine

◦ NE storage in synaptic vesicles

◦ Release of NE (еxocytosis) with the participation of Ca2+

◦ Binding to and activation of c- receptors
◦ Postsynaptic receptors – effect
◦ Presynaptic α2 receptors –
decrease of NE release

◦ Uptake of NE by NET or to a less
extent – diffusion

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2
Q

What are the possible ways to affect adrenergic transmission?

A

◦ Metyrosine inhibits tyrosine
hydroxylase

◦ Reserpine alkaloids inhibit vesicular
monoamine transporter (VMAT)

◦ Bretylium, guanetidine inhibit NE
release

◦ Cocaine and certain antidepressant
drugs inhibit norepinephrine
transporter (NET)

◦ MAO inhibitors and COMT
inhibitors inhibit the metabolism of
NE

◦ Receptor agonists and antagonists

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3
Q

Which are the adrenoreceptors involved in the ANS?

A
  • Alpha 1
  • Alpha 2
  • Beta 1
  • Beta 2
  • Beta 3
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4
Q

Where are alpha 1 receptors localized and what type of cellular response do they elicit?

A

Alpha1

Postsynaptic effector cells, especially smooth
muscle

GPCR (Gq)
↑ IP3, DAG,
Increased intracellular Ca2+

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5
Q

Where are alpha 2 receptors localized and what type of cellular response do they elicit?

A

Alpha2

Presynaptic adrenergic nerve terminals,
platelets, smooth muscle

GPCR (Gi)
Inhibition of AC, ↓ cAMP

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6
Q

Where are beta 1 receptors localized and what type of cellular response do they elicit?

A

Beta1

Postsynaptic effector cells, especially heart,
brain; presynaptic adrenergic and cholinergic
nerve terminals, juxtaglomerular apparatus of
renal tubules, ciliary body epithelium

GPCR (Gs)
Stimulation of AC, ↑ cAMP

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7
Q

Where are beta 2 receptors localized and what type of cellular response do they elicit?

A

Beta2

Postsynaptic effector cells, especially smooth
muscle

GPCR (Gs)
Stimulation of AC, ↑ cAMP

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8
Q

Where are beta 3 receptors localized and what type of cellular response do they elicit?

A

Beta3

Postsynaptic effector cells, especially lipocytes

GPCR (Gs)
Stimulation of AC, ↑ cAMP

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9
Q

Where are dopamine receptors localized and what type of cellular response do they elicit?

A

D1
(DA1)

Brain; effector tissues, especially smooth
muscle of the renal vascular bed

GPCR (Gs)
Stimulation of AC, ↑ cAMP

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10
Q

Which receptors are present in the eye and what action does the neurotransmitter elicit?

A

Receptors:
α1
β
α2

Eye:
Iris radial muscle -> Contracts

Epithelium of the ciliary
body

↑ secretion of
aqueous humor
↓ secretion of
aqueous humor

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11
Q

Which receptors are present in the heart and what action does the neurotransmitter elicit?

A

Sinoatrial node
Ectopic pacemakers
Contractility

β1
β1
β1

Accelerates
Accelerates
Increases

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12
Q

Which receptors are present in the blood vessels and what action does the neurotransmitter elicit?

A

Blood vessels:

1) Skin, splanchnic vessels
2) Skeletal muscle vessels

1) α
2) β2

1) Contracts
2) Relaxes

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13
Q

Which receptors are present in the bronchiolar smooth muscles and what action does the neurotransmitter elicit?

A

Bronchiolar smooth muscle β2

Relaxes

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14
Q

Which receptors are present in the GIT (smooth muscle) and what action does the neurotransmitter elicit?

A

Gastrointestinal tract – Smooth
muscle:

Walls
Sphincters

α2
α1

Relaxes
Contracts

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15
Q

Which receptors are present in the Genito-urinary tract and what action does the neurotransmitter elicit?

A

Genitourinary smooth muscle:

Bladder wall -> β2 = relaxes
Sphincter -> α1 = contracts
Uterus, pregnant -> β2 = relaxes
α = contracts

Prostate capsule -> α1 = contracts
Penis, seminal vesicles -> α = ejaculation

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16
Q

Which receptors are present in the skin and what action does the neurotransmitter elicit?

A

Pilomotor smooth muscle
Sweat glands
-Eccrine
-Apocrine (stress)

α
M
α

Contracts
Increases
Increases

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17
Q

Which receptors are present in the pancreas and what action does the neurotransmitter elicit?

A

Pancreas

α2 =↓ insulin
β2 =↑ insulin

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18
Q

Which receptors are present in the kidney and what action does the neurotransmitter elicit?

A

β1 ↑ renin

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19
Q

Which receptors are present on the mast cells and what action does the neurotransmitter elicit?

A

β2 ↓ Histamine

release

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20
Q

Which receptors are present in the presynaptic membrane in nerve endings and what action does the neurotransmitter elicit?

A

α2 ↓ NE release

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21
Q

Which receptors are present in organs with metabolic functions like the liver and fat cells and what action does the neurotransmitter elicit?

A

Liver -> β2, α = Gluconeogenesis

Liver -> β2, α = Glycogenolysis

Fat cells -> β3 = Lipolysis

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22
Q

How are the drugs affecting adrenergic transmission classified?

A
  1. Alpha adrenomimetics
  2. Alpha-adrenoceptor antagonists
  3. Beta- adrenoceptor agonists
  4. beta-adrenoceptor antagonists
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23
Q

What is a direct-acting, non-selective, alpha-adrenoceptor agonist?

A

Epinephrine

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24
Q

What is the PK of Epinephrine (direct-acting, non-selective, alpha-adrenoceptor agonist)?

A

◦ Orally inactive (metabolism by COMT and MAO in the GIT)

◦ Parenteral administration: SC, slow IV, locally (with local anesthetics)

◦ Short plasma half-life

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25
Q

What are the effects of epinephrine?

A

◦ Mydriasis (α1)

◦ CVS

◦ Cardiac stimulation (beta1)

◦ Vasoconstriction (α1) and vasodilation in skeletal muscles (beta2)

◦ Slight increase of mean BP (α1,beta2), sometimes decrease of diastolic BP (beta2)

◦ Respiratory system

◦ Bronchodilation (beta2)

◦ Anti-allergic effects (↓ release of histamine from mast cells) (beta2)

◦ ↑ blood glucose (beta2, α1)

◦ Hypokalemia (beta2)

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26
Q

What are the clinical uses of Epinephrine?

A

◦ In emergencies:

◦ Anaphylactic shock and other acute hypersensitivity reactions
◦ Hypoglycemic coma
◦ Status asthmaticus (acute exacerbation of asthma that remains
unresponsive to initial treatment with bronchodilators)
◦ Cardiac arrest

◦ To prolong the effect of local anesthetics

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27
Q

What are the adverse reactions of Epinephrine?

A 
◦ Tachycardia, arrhythmia
◦ Increased O2
consumption by the heart
◦ Hyperglycemia
◦ Hypokalemia
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28
Q

What are the PK, PD, and clinical uses of norepinephrine?

A

PK
◦ Parenteral administration; short duration of action

PD
◦ Vasoconstriction (1)
◦ Increase of peripheral vascular resistance; an increase of systolic and diastolic BP

Clinical use
◦ In combination with local anesthetics

29
Q

What are the PK and the clinical use for midodrine?

A

PK
◦ Oral administration
◦ Longer duration of action

Clinical use
◦ Hypotension

30
Q

What is the mode of administration and adverse reactions of xylomethazoline?

A

Local administration in
the nose in:
◦ Rhinitis

ADR:
◦ With prolonged use: atrophic
rhinitis and anosmia (loss of
the sense of smell)

31
Q

Which are the alpha 2 selective direct-acting, alpha-adrenoceptor agonists?

A

Systemic:

  • Clonidine
  • Methyldopa

Local - for treatment of glaucoma
- Brimonidine

32
Q

What are the PK, PD, clinical use, and adverse reactions of Clonidine ?

A

PK
◦ Oral administration (Clonidine, methyldopa)
◦ By injection (Clonidine)

PD
◦ In CNS: Decrease of the sympathetic tone
◦ In the peripheral tissues: decrease the release of NE (a2)

Clinical use
◦ Hypertension
◦ Migraine prophylaxis (Clonidine)
◦ Treatment of drug dependence

ADR: 
◦ Sedation, drowsiness, depression
◦ Xerostomia (Clonidine)
◦ Bradycardia, AV block(Clonidine)
◦ Rebound effect (Clonidine)
33
Q

What are the PK, PD, clinical use, and adverse reactions of Methyldopa?

A

PK
◦ Oral administration (Clonidine, methyldopa)
◦ By injection (Clonidine)

PD
◦ In CNS: Decrease of the sympathetic tone
◦ In the peripheral tissues: decrease the release of NE (a2)

Clinical use
◦ Hypertension
◦ In pregnant women (Methyldopa)
◦ Treatment of drug dependence

ADR
◦ Sedation, drowsiness, depression
◦ Тhombocytopenia (Methyldopa)
◦ Parkinsonism (Methyldopa)
◦ Liver disorders (Methyldopa)
34
Q

What are the PD and clinical use of Brimonidine?

A

PD
◦ In the eye: lowers
intraocular pressure

Clinical use
◦ Glaucoma

35
Q

What is the PK, mechanism of action, effects, and clinical significance of amphetamine?

A

PK
◦ Orally active; penetrates through the BBB

Mechanism of action (indirect action):
◦ Releases NE, at high doses – dopamine and serotonin, as well

Effects:
◦ Cardio-vascular stimulation
◦ CNS:
◦ Mental stimulation and exercise; increased caution
◦ Euphoria
◦ Appetite suppression (suppression of the center of hunger)

Clinical significance - limited:
◦ Narcolepsy
◦ Attention deficit hyperactivity disorder

36
Q

What are the PK, PD, adverse effects, desired effects, and clinical significance of Ephedrine?

A 
PK
◦ Orally active
◦ Renal excretion
◦ Slower onset and longer duration of action in comparison with
epinephrine: effect lasting 4-6 hours

PD
• Mechanism of action – mixed action
◦ Indirect: release of NЕ (predominantly -effects)
◦ Direct: on β-adrenergic receptors
• Effects – similar to those of epinephrine

ADR: 
◦ CNS stimulation (insomnia)
◦ Tachyphylaxis – depletion of NE
Clinical significance - limited:
◦ Bronchial asthma
◦ As a bronchodilator
◦ Arterial hypotension
◦ Rhinitis
37
Q

What is pseudoephedrine used for?

A

As a component of the
solutions with a
decongestant action in
rhinitis

38
Q

How are the alpha-adrenoceptor antagonists classified?

A

Non-selective

Selective a1

39
Q

What is Nicergoline?

A

Non-selective (α1, α2) antagonists

40
Q

Which are the alpha 1 selective alpha-adrenoceptor antagonists?

A

Prazosin, Doxazosin, Tamsulosin

41
Q

What are the PK, PD, adverse reactions, and clinical use of Prazosin, Doxazosin, and Tamsulosin?

A

PK
◦ Oral administration
◦ Prazosin t1/2 = 3 h; effect – 6-8 h: 3 times daily
◦ Tamsulosin t1/2 = 9-15 h; prolonged-release tablets: once daily
◦ Doxazosin t1/2 = 22 h; once daily

PD
◦ ↓ peripheral vascular resistance (predominantly arterial vasodilation); ↓ BP
◦ ↑HDL and ↓LDL (with chronic use)
◦ Relaxation of the smooth muscle of the prostate capsule

ADR:
◦ Orthostatic hypotension; “Effect of the first dose” – prazosin
◦ Tachycardia
◦ Sexual disturbances: ↓ ejaculation
◦ Nasal congestion

Clinical use:
◦ Hypertension: prazosin, doxazosin
◦ Benign prostate hyperplasia: doxazosin, tamsulosin (tamsulosin selective α1A)

42
Q

What are the PK and PD of dopamine?

A

PK: IV administration

PD:
• D1 receptor agonist: vasodilation of renal,
splanchnic, coronary, brain vessels
• Renal effects – used clinically to improve
the perfusion to the kidneys in situations
of oliguria
• β1 receptor agonist in the heart
• Activation of vascular α receptors (at
higher rates of infusion) vasoconstriction,
including in the renal vascular bed.
Consequently, high rates of infusion of
dopamine may mimic the actions of
epinephrine.

43
Q

What is isoprenaline?

A

Very powerful agonist of β receptors:

• β1 – positive chrono- and inotropic
effect; ↑ cardiac output; slight ↑ systolic
BP
• β2 – vasodilation; ↓ diastolic BP

Clinical use:
• АV block

44
Q

What is Dobutamine?

A

Synthetic catecholamine

45
Q

What are the PK, PD, clinical uses, and adverse reactions of dobutamine?

A

PK:
• IV infusion

PD:
• Relatively β1-selective
• Effects:
◦ β1: Cardiac stimulation
◦ Inotropic (most pronounced, comparable to that of epinephrine)
◦ Bathmotropic effect (weaker than that of epinephrine)
◦ Weak α1
-adrenomimetic effect - in higher doses

Clinical use:
◦ Cardiogenic shock
◦ Acute heart failure

ADR:
◦ Arrhythmia
◦ ↑ O2
consumption (symptoms of angina pectoris)

46
Q

What are examples of short-acting beta 2 selective beta-adrenoceptor agonists?

A

Salbutamol, Hexoprenaline, Clenbuterol

PK
◦ Route of administration:
◦ Inhalation (in asthma)
◦ Orally or by injection (in obstetrics and gynecology)
◦ Бъбречна екскреция
◦ t1/2 ~ 4 ч.
PD
◦ Bronchodilation
◦ Relaxation of the uterus
◦ Vasodilation in skeletal muscles
◦ Anabolic effect:
◦ Vascular effects of the compounds that should modify the nutrient flow into the
muscle
◦ Beta-adrenergic-dependent enhancement of insulin action on the muscle

Clinical use
◦ Bronchial asthma attack
◦ To prevent premature labor

ADR
◦ Tachycardia
◦ Tremor
◦ Hypokalemia (increased penetration of K into the cells)
◦ Hypotension
47
Q

What are examples of long-lasting beta 2 selective, beta-adrenoceptor agonists?

A

Salmeterol,
Formoterol

PK
◦ Route of administration:
◦ Inhalation – once daily
◦ Long duration of action
(longer with Salmeterol)

PD
◦ Bronchodilation

Clinical use
◦ Bronchial asthma (chronic
use, always with GCS)

ADR
◦ Worsening of asthma if
administered alone

48
Q

How are the beta-adrenoceptor antagonists classified?

A
  1. Non-selective (β1, β 2)
    Propranolol
    Sotalol
  2. β1-selective (cardioselective)
    Atenolol
    Bisoprolol
    Metoprolol
  3. Vasodilating
    Carvedilol
    Nebivolol
  4. For treatment of glaucoma
    Timolol (non-selective)
    Betaxolol (beta1-selective)
49
Q

What are the lipid solubility, oral-bioavailability, elimination, and half-life of propranolol?

A

Lipid Solubility: ++
Oral bioavailability: 30%
Elimination: liver - first-pass metabolism, active metabolite
Half-life: 3-5 h

50
Q

What are the lipid solubility, oral-bioavailability, elimination, and half-life of atenolol?

A

Lipid Solubility: -
Oral bioavailability: 40%
Elimination: renal
Half-life: 3-4 h

51
Q

What are the lipid solubility, oral-bioavailability, elimination, and half-life of metoprolol?

A

Lipid Solubility: ++
Oral bioavailability: 50%
Elimination: liver
Half-life: 3-4 h

52
Q

What are the lipid solubility, oral-bioavailability, elimination, and half-life of bisoprolol?

A

Lipid Solubility: ++
Oral bioavailability: 90%
Elimination: 50% in liver, 50% renal
Half-life: 9-12 h

53
Q

What are the lipid solubility, oral-bioavailability, elimination, and half-life of carvedilol?

A

Lipid Solubility: +
Oral bioavailability: 25-35%
Elimination: liver, active metabolite
Half-life: 7-10h

54
Q

What are the lipid solubility, oral-bioavailability, elimination, and half-life of nebivolol?

A

Lipid Solubility: +
Oral bioavailability: 12-96%
Elimination: liver
Half-life: 11-30h

55
Q

What is the pharmacodynamics of Propanolol?

A

non-selective, local anesthetic effect

56
Q

What is the pharmacodynamics of timolol?

A

beta-blocker used in the treatment of glaucoma

no local anesthetic effect

57
Q

What is the pharmacodynamics of atenolol?

A

beta 1 selective beta-blocker

no local anesthetic effect

58
Q

What is the pharmacodynamics of metoprolol?

A

beta 1 selective beta-blocker

local anesthetic effect

59
Q

What is the pharmacodynamics of betaxolol?

A

beta 1 selective bab

weak local anesthetic effect

60
Q

What is the pharmacodynamics of bisoprolol?

A

great beta 1 selective beta-blocker

no anesthetic effect

61
Q

What is the pharmacodynamics of carvedilol?

A

vasodilating beta blocker

block receptors

no local anesthetic effect

62
Q

What is the pharmacodynamics of nebivolol?

A

beta 1 selective beta-blocker

NO release (mechanism of action)

no local anesthetic effect

63
Q

What are the effects of BAB on the CVS?

A

Effects on the CVS:

◦ Heart
◦ ↓ heart rate
◦ ↓ contractility (stroke volume)
◦ As a result of these: ↓ cardiac output; ↓ BP

◦ Blood vessels
◦ ↑ peripheral vascular resistance (nonselective)
◦ ↓ peripheral vascular resistance
(vasodilating)

◦ Kidneys
◦ ↓ renin release

64
Q

What are the effects of BABs on the respiratory system?

A

Respiratory system:

• Bronchoconstriction (nonselective)

65
Q

What are the metabolic effects of BABs?

A

Metabolic effects:

◦ Carbohydrate metabolism
◦ Severe hypoglycemia is possible
during insulin therapy
◦ Masked hypoglycemia
◦ Insulin resistance (with chronic use)
◦ Lipid metabolism (chronic
administration of non-selective
BAB)
◦ ↑ VLDL
◦ ↓ HDL
66
Q

What are the adverse reactions of BABs?

A 
ADR
◦ Bronchoconstriction (in
asthma, particularly nonselective)
◦ Cold extremities (β2)
◦ Nightmares, depression (in
lipophilic BAB)
◦ Bradycardia, AV block
◦ Impotence (male)
◦ Rebound effect
◦ Metabolic effects (with
chronic use)
67
Q

What are the contraindications of BABs?

A 
Contraindications
◦ Bronchial asthma
◦ Peripheral vascular disease
◦ AV block and bradycardia
◦ Acute heart failure
68
Q

What are the drug interactions of BABs?

A 
Drug interactions
◦ Contraindicated combination: with
verapamil: both drugs ↓ heart rate
and contractility
◦ Useful combinations: with nitrates or
DHP calcium channel blockers: in
myocardial ischemia and
hypertension
69
Q

What are the clinical uses of BABs?

A

Cardiovascular indications:

◦ Hypertension

◦ Ischemic heart disease

◦ Acute myocardial infarction – early (4-6 h after the infarction – limitation of the
infarction size, prevention of arrhythmias)

◦ Tachyarrhythmia

◦ Chronic heart failure (metoprolol, bisoprolol, carvedilol, nebivolol)

Other indications
◦ Thyrotoxicosis
◦ Tremor
◦ Migraine – prophylactically (propranolol)
◦ Glaucoma (timolol, betaxolol)

Pharmacology (35 decks)

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