1. Sympathetic
Nervous System

2. Nervous System CNS PNS Brain Spinal Cord Autonomic NS Somatic NS
Sympathetic
Parasympathetic

3. CNS
ACh C M N
ACh T
ACh 1 NE N L NE 1 2 S
ACh SM N

4. CNS
ACh C M N
ACh T
ACh 1 NE N L NE 1 N
EPI
ACh 2 S
ACh SM N

5. CNS
ACh C M N
ACh T
ACh 1 NE N L NE
ACh N 1
ACh SG M 2 S
ACh SM N

6. Sympathetic Nervous System
CNS
(-) 2 C M T
ACh 1 NE N L NE 1 N
EPI
ACh 2 S

7. Dual Innervation Predominant Tone
Exceptions
(only sympathetic)
- blood vessels
(only parasympathetic)
- bronchioles
- ciliary muscles
(only parasympathetic)
Predominant Tone
Primarily parasympathetic NS
Exceptions
- blood vessels (sympathetic)
- sweat glands (sympathetic cholinergic)

8. Denervation Supersensitivity
+ Effect
+++ Effect NT NT
Before Denervation
After Denervation

9. Catecholamines NE
EPI DA

12. NE - predominately removed from synapse via ‘re-uptake 1’
PRESYNAPTIC
POSTSYNAPTIC
NE - predominately removed from synapse via ‘re-uptake 1’
Metabolic Removal
Re-uptake 2
Re-uptake 1
NE synthesis
COMT
MAO NE
MAO NE
 / 
Action
(-) 2
Receptor
Binding

13. Drug actions at presynaptic autonomic nerve terminals

14. Adrenergic Receptors
1, 2, 1 NE
1, 2, 1, 2
EPI

15. Adrenergic Receptors
1, 2, 1 NE
1, 2, 1, 2
EPI
1, 1, DA1 DA

16. TACHYCARDIA and INCREASED BRONCHORELAXATION (2)
EFFECTS OF STIMULATING ADRENERGIC RECEPTORS
SITE EFFECT
HEART
TACHYCARDIA and INCREASED
CONTRACTILITY (1)
VASCULATURE
VASODILATION
VASOCONSTRICTION
(2)
(1,  2)
AIRWAYS
BRONCHORELAXATION (2)
IRIS
MYDRIASIS (1)
BLADDER
DECREASED URINATION (2)
GI TRACT
DECREASED GI MOTILITY and SECRETIONS (2)
UTERUS
RELAXATION (2)

17. 1 2 1, 2 vasodilation, contractile force heart rate renin release
TPR 2
vasoconstriction
TPR
1, 2

18. Drugs and Adrenergic Synapses

19. Adrenergic Agonists SM
CNS
Adrenergic Agonists
ACh C M N
ACh T
ACh 1 NE N L NE 1 N
EPI
ACh 2 S
ACh SM N

20. MIXED ADRENERGIC AGONISTS
Norepinephrine
1, 2, 1
Epinephrine
1, 2, 1, 2
Dopamine
DA1, 1, 1

21. HR BP
TPR

22. Norepinephrine (1, 2, 1) Epinephrine (1, 2, 1, 2)
MIXED ADRENERGIC AGONISTS
Norepinephrine (1, 2, 1)
Epinephrine (1, 2, 1, 2)
Tx: ● Asthma (but there are better drugs)
● Anaphylactic shock
● Cardiogenic shock
● Prolong action of local anesthetics
● Topical hemostatic agent
Dopamine (DA, 1, 1)
Tx: ● CHF

23. ALPHA AGONISTS - Phenylephrine (1) - Methoxamine (1)
- Oxymetazoline (1 and 2 in periphery)
- Tetrahydrozoline (1)
- Naphazoline (1)
- Ephedrine/Pseudoephedrine (1)
- Clonidine (2, Tx site of action is CNS)

24. Tx uses for ALPHA AGONISTS Alpha-1 agonists Alpha-2 agonists
Tx: ● Nasal decongestion
● Used in eye drops to ‘get the red out’
● Hypotensive states
Alpha-2 agonists
Tx: ● Hypertension

25. BETA AGONISTS and Tx uses
Non-selective 1/2
- Isoproterenol
Selective 1
- Dobutamine
Selective 2
- Albuterol
Tx: Cardiac stimulant
- Metaproterenol
Tx: COPD,
Asthma
- Terbutaline
- Isoetharine
- Bitolterol
Tx: Inotropic agent
Tx:
Uterine relaxation
- Ritodrine

26. NE
EPI
ISO HR BP
TPR

27. Dose-response effects produced by dopamine at different receptors

28. CNS : Tx antihypertensive effect
CNS ADRENERGIC AGENTS
CNS : Tx antihypertensive effect
- Clonidine (2 agonist)
- Guanabenz (2 agonist)
- Guanfacine (2 agonist)
- Methyldopa
Converted in CNS to methylnorepinephrine
(low efficacy 2 agonist)

29. Sympathetic Nervous System
CNS
(-) 2 C M T
ACh 1
(-) NE N
(-) L NE N 1
EPI
ACh 2 S 2

30. Adrenergic Antagonists
CNS
Adrenergic Antagonists
ACh C M N
ACh T
ACh 1 X NE N L X NE 1 N
EPI X
ACh 2 S
ACh SM N

31.  Nonselective 1 and 2 receptor antagonists
ALPHA ANTAGONISTS
and Tx uses
 Nonselective 1 and 2 receptor antagonists
- Phenoxybenzamine
Non-competitive action
- Phentolamine
Competitive action
Tx: - DOC for overdose of alpha agonists
- Management of pheochromocytoma
- Dental use for reversal of local anesthetic action
 Selective 1 receptor antagonists
- Prazosin
- Terazosin (water soluble)
Tx: Antihypertensive agents,
Management of benign prostatic hypertrophy

32. Adrenergic Influence on Vascular Smooth Muscle Tone
VSMC 2 NE NE 1
Vasoconstriction
(-) 2

33. Adrenergic Influence on Vascular Smooth Muscle Tone
EPI
VSMC 2
Vasoconstriction NE NE 1
Vasoconstriction
(-) 2

34. X X X Vasodilation Vasodilation (-)
Marked hypotensive response produced by dual
1 and 2 - Receptor Blockade on VSMC
EPI X
VSMC 2
Vasodilation NE X NE 1
Vasodilation
(-) X 2
Phentolamine - 1 and 2 blockade

35. X Vasodilation (-) Moderate hypotensive response produced by dual
1 and 2 - Receptor Blockade 0n VSMC
EPI
VSMC 2
Vasoconstriction NE X NE 1
Vasodilation
(-) 2
Prazosin - selective 1 blockade

36. ● ‘Cardio’- Selective 1
BETA ANTAGONISTS
● Non-selective 1, 2
● ‘Cardio’- Selective 1
Atenolol
Propranolol
Metropolol
Nadolol
Esmolol
Timolol
Acebutolol (ISA)
Pindolol
● Non-selective
1, 2, 1
Carteolol
Intrinsic
Sympathomimetic
Activity
Labetalol
Carvedilol

37. ● Congestive heart failure ● Myocardial infarction
Beta Blocker Tx Uses:
● Hypertension
● Congestive heart failure
● Myocardial infarction
● Angina
● Migrane
● Arrhythmias
● Anxiety
● Stage fright

38. INDIRECT ACTING ADRENERGIC Tyramine (dietary substance)
AGONISTS
Tyramine (dietary substance)
Ephedrine
Pseudoephedrine
Amphetamine

39. Amphetamine Action PRESYNAPTIC POSTSYNAPTIC Re-uptake 1 NE  / 
Receptor
Binding

40. NE Amphetamine amphetamine Action PRESYNAPTIC POSTSYNAPTIC Re-uptake 1
(+)
 / 
Action
Receptor
Binding

41. Tricyclic Antidepressants
Uptake Blockers
Cocaine
Tricyclic Antidepressants

42. Cocaine Action PRESYNAPTIC POSTSYNAPTIC Re-uptake 1 NE  /  Receptor
Binding

43. X NE Cocaine cocaine Action PRESYNAPTIC POSTSYNAPTIC Re-uptake 1  / 
Receptor
Binding

44. Neuronal Blockers Reserpine Guanethadine
Depletes NE stores by inhibiting vesicular uptake of NE; NE then metabolized by intra-neuronal MAO
Guanethadine
Inhibits NE release, also causes NE depletion, and can damage NE neurons

45. Monoamine Oxidase (MAO) Inhibitors
Pargyline
Tranylcypromine
Tyramine (or other drugs that promote NE release) may cause markedly increased blood pressure in patients taking MAO inhibitors