The document provides an overview of the autonomic nervous system, describing the two divisions of the sympathetic and parasympathetic nervous systems. It explains the neurotransmitters involved, including acetylcholine and norepinephrine, and the receptors they act on. The document also discusses the classes of drugs that act on the autonomic nervous system, including direct-acting cholinergic agonists, indirect-acting cholinergic agonists that inhibit acetylcholinesterase, and antimuscarinic drugs that block muscarinic receptors.

1. Introduction to
Autonomic Nervous System
1
Pharmacology Team
Naim Kittana, Suhaib Hattab, Ansam Sawalha, Adham Abu Taha,
Waleed Sweileh, Ramzi Shawahneh
Faculty of Medicine & Health Sciences
An-Najah National University

2. Nervous system’s branches
2

3. Comparison of efferent nervous system branches
Epi and NE are release in the circulation and activate
adrenergic receptors
Ach: acetylcholine
N: Nicotinic receptors
M: Muscarinic receptors
Epi: Epinephrine
NE: Norepinephrine
D: dopamine
D1: Type 1 D receptors
Preganglionic
neuron
Postganglionic
neuron
Adopted with modifications from: http://pharmacology-
online.blogspot.com/2011/04/neurotransmitter-chemistry-of-autonomic.html
No ganglia
Sympathetic
chain ganglia
3

4. • Acetylcholine is the neurotransmitter of:
– Preganglionic nerves of both parasympathetic and sympathetic nervous
system
– Postganlionic nerves of parasympathetic nerves system
– Postganlionic nerves of sympathetic nervous system supplying sweat
glands
– Preganglionic fibers terminating in the adrenal medulla
• Norepinephrine is the major neurotransmitter of postganglionic nerves of
sympathetic system.
• Dopamine: is the neurotransmitter of postganglionic nerves of
sympathetic system supplying the renal smooth muscles.
Transmitters of autonomic nervous system (ANS)
4

5. Note on Cholinergic neurons in the CNS:
– Alzheimer disease: a significant loss of cholinergic neurons
in the temporal lobe and entorhinal cortex.
– Most of the drugs available to treat the disease are
acetylcholinesterase (AChE) inhibitors.
5

6. • Parasympathetic NS:
– Midbrain – III cranial nerve.
– Medulla – VII, IX and X cranial nerve.
– Sacral part of spinal cord – S - 2, 3, 4
• Sympathetic NS:
The preganglionic fibers originate from the thoracolumbar
region of the spinal cord.
Origins of preganglionic neurons of ANS
6

7. 7

8. 8

9. • Two groups of ANS drugs:
1. The cholinergic drugs: acetylcholine (ACh) receptors
2. The adrenergic drugs: adrenergic receptors
9

10. Cholinergic Agonists
10

11. 11

12. Cholinergic agonists
AchE: Acetylcholinesterase
12

13. Neurotransmission at cholinergic neurons
• Six sequential steps:
1. Synthesis of ACh by Choline
acetyltransferase (ChAT)
2. Storage
3. Release
4. Binding of ACh to a receptor
5. Degradation of the
neurotransmitter in the
synaptic cleft by
acetylcholinesterase (AChE)
6. Recycling of choline
https://www.studyblue.com/
13

14. Cholinergic receptors (Cholinoceptors)
• Two families of cholinoceptors
A. Muscarinic
B. Nicotinic
14

15. 15

16. DIRECT-ACTING CHOLINERGIC AGONISTS
(Parasympathomimetics)
• Mimic the effects of ACh by binding directly to cholinoceptors.
• Broadly classified into two groups:
1. Choline esters include:
– Ach
– Synthetic esters of choline such as Carbachol and
Bethanechol.
2. Naturally occurring alkaloids, such as pilocarpine.
• All have longer durations of action than ACh.
16

17. • muscarinic agents: (pilocarpine and bethanechol)
preferentially bind to muscarinic receptors
• They show little specificity in their actions, which limits their
clinical usefulness.
DIRECT-ACTING CHOLINERGIC AGONISTS
(Parasympathomimetics)
17

18. Actions of Direct-Acting Cholinoceptor Agonists
18

19. Therapeutic uses of Pilocarpine:
1. Treatment of glaucoma
• The drug of choice in the emergency lowering of intraocular
pressure of both:
– Narrow-angle (or closed-angle)
– Wide-angle (also called open-angle) glaucoma
19

20. Mechanism of glaucoma treatment by Pilocarpine
20

21. • Mechanism of glaucoma treatment by Pilocarpine:
 Contracting the smooth muscle of iris sphincter
(contraction of pupil)
 Iris pulled away from angle of anterior chamber
 Contraction of ciliary muscle
 Widening the filtration angle and opening the trabecular
network
 Increased outflow of aqueous humour
----> decreased intraocular pressure
• Onset of action: few minutes
• Duration of action: 4 to 8 hours
21

22. 2. The miotic action of pilocarpine is also useful in reversing
mydriasis due to atropine (antimuscarinic drug).
3. Pilocarpine is used to promote salivation, useful for:
– Patients with Xerostomia (dry mouth) from different
underlying causes including treatment of Sjögren’s
syndrome, which is characterized by dry mouth and lack of
tears.
Therapeutic uses of Pilocarpine:
22

23. 23

24. Indirect-acting Cholinomimetic
(Cholinergic) Drugs
Organophosphate
(Very long-acting)
Edrophonium
(Short acting)
Carbamates
(Intermediate-acting)
Physostigmine
Neostigmine
Pyridostigmine
Ambenonium
Tacrine
Donepezil
Rivastigmine
Galantamine
Ecothiophate
Parathion (insecticide)
Nerve gases: Tabun,
Sarin, and Soman
Reversible
inhibitors
24

25. Indirect-acting cholinergic agonists:
acetylcholinesterase inhibitors (reversible)
• Acetylcholinesterase (AChE) cleaves ACh to acetate and
choline and, thus, terminates its actions.
• It is located both pre- and postsynaptically in the nerve
terminal where it is membrane bound.
• Inhibitors of AChE results in the accumulation of ACh in the
synaptic space.
• The reversible AChE inhibitors can be classified as:
– short-acting agents
– intermediate-acting agents.
25

26. 26

27. Short-acting indirect cholinergic agonist
27

28. Edrophonium
• The prototype short-acting AChE inhibitor.
• Edrophonium binds reversibly to the active center of AChE,
preventing hydrolysis of ACh.
• It is rapidly absorbed
• Short duration of action: 10 to 20 minutes, due to rapid renal
elimination.
• Edrophonium is a quaternary amine, and its actions are limited to
the periphery.
28

29. Clinical uses of Edrophonium
1. Diagnosis of myasthenia gravis
29

30. • Myasthenia gravis, which is an autoimmune disease caused by
antibodies against the nicotinic receptor at NMJs, resulting in
their degradation, so that fewer receptors are available for
interaction with the ACh.
• Intravenous injection of edrophonium leads to a rapid
increase in muscle strength.
30
Clinical uses of Edrophonium

31. 2. Edrophonium may also be used to assess cholinesterase
inhibitor therapy, for differentiating cholinergic and myasthenic
crises.
3. Reversing the effects of “nondepolarizing neuromuscular
blockers” after surgery.
• Due to the availability of other longer-acting agents,
edrophonium use has become limited.
31
Clinical uses of Edrophonium

32. Intermediate-acting indirect cholinergic agonist
32

33. Physostigmine
• Found naturally in plants
• A tertiary amine.
• It is a substrate for AChE, and it forms a relatively stable
carbamoylated intermediate with the enzyme, which then
becomes reversibly inactivated.
• The result is potentiating the cholinergic activity throughout
the body.
33

34. Some actions of Physostigmine
Contraction of visceral
smooth muscles
Miosis
Hypotension
Bradycardia
34

35. Neostigmine reversibly inhibits AChE in similar to that of
physostigmine.
Actions:
• A quaternary nitrogen, more polar, absorbed poorly from
the GI tract, and does not enter the CNS.
• Its effect on skeletal muscle is greater than that of
physostigmine.
• Intermediate duration of action: 30 minutes to 2 hours.
Neostigmine
35

36. Therapeutic uses of Neostigmine:
a) It stimulates the bladder and GI tract
a) An antidote for tubocurarine and other competitive
neuromuscular-blocking agents.
b) Used to symptomatically treat myasthenia gravis.
36

37. Symptoms of generalized cholinergic stimulation, such as :
• Salivation
• Flushing
• Decreased blood pressure
• Nausea, abdominal pain and diarrhea
• Bronchospasm
Note: Neostigmine does not cause CNS side effects, and is not
used to overcome toxicity of central-acting antimuscarinics
like Atropine
37
Adverse effects of Neostigmine:

38. Pyridostigmine and Ambenonium
• Clinical Use: chronic management of myasthenia gravis.
• Durations of action (intermediate):
–3 to 6 hours : pyridostigmine
–4 to 8 hours: ambenonium
• Adverse effects: similar to those of neostigmine.
38

39. Tacrine, Donepezil, Rivastigmine, and
Galantamine
• Centrally acting reversible acetylcholinesterase inhibitors
• Clinical use: Treatment of Alzheimer disease symptoms
• Tacrine has been replaced by other drugs because it is
hepatotoxic
• Can delay the progression of Alzheimer disease, none can
stop its progression.
• Side effects: primarily GI distress
39

40. Long-acting indirect cholinergic agonist
(irreversible)
40

41. Indirect-acting cholinergic agonists:
anticholinesterases (irreversible)
• A number of synthetic organophosphate compounds have the
capacity to bind covalently to AChE.
• The result is a long-lasting increase in ACh at all sites where it is
released.
• Many of these compounds are extremely toxic and were developed
by the military as nerve agents.
• Related compounds, such as parathion, are used as insecticides.
• Few compounds have clinical use (e.g. Echothiophate)
41

42. Mechanism of action:
• Organophosphates covalently bind via its phosphate group to the
serine-OH group at the active site of AChE.
• Once this occurs, the enzyme is permanently inactivated, and
restoration of AChE activity requires the synthesis of new enzyme
molecules.
• Following covalent modification of AChE, the phosphorylated
enzyme slowly releases one of Organophosphates ethyl groups.
• The loss of an alkyl group, which is called aging, makes it
impossible for chemical reactivators, such as pralidoxime, to break
the bond between the remaining drug and the enzyme.
42

43. • Echothiophate produces intense miosis when applied topically
as an ophthalmic solution.
• It can decrease the intraocular pressure (IOP) by facilitating the
outflow of aqueous humor.
• Clinical use: chronic treatment of open-angle glaucoma.
• It is not a first-line agent because it can cause cataract
Therapeutic uses of Echothiophate
43

44. Toxicology of acetylcholinesterase inhibitors
• AChE inhibitors are commonly used as agricultural insecticides
• Numerous cases of accidental intoxication with these agents.
• Toxicity with these agents is manifested as nicotinic and
muscarinic signs and symptoms.
44

45. Symptoms of intoxication with organophosphates
• Ophthalmic symptoms: Miosis, ocular pain, conjunctival
congestion, diminished vision, lacrimation
• Upper respiratory tract symptoms: Rhinorrhea, tightness in
the chest and wheezing respiration, caused by the
combination of bronchoconstriction and increased bronchial
secretion
• GI symptoms: extreme salivation, nausea and vomiting,
abdominal cramps, diarrhea and involuntary defecation.
45

46. Symptoms of intoxication with organophosphates
• CV symptoms: Bradycardia, and hypotension
• CNS symptoms: Confusion, ataxia, slurred speech, loss of
reflexes, generalized convulsions, coma, and central
respiratory paralysis
• Excessive sweating and involuntary urination
• Severe weakness and paralysis of skeletal muscles
46

47. • Reactivation of AChE: by administration of Parlidoxime
• Atropine in high dosages can reverse many of the muscarinic
and some of the central effects of organophosphates, such as
increased bronchial secretion and salivation,
bronchoconstriction, and bradycardia.
• Diazepam is also administered to reduce the persistent
convulsion caused by these agents.
Management of organophosphates toxicity
47

48. • General supportive measures, such as:
– Maintenance of patent airway
– Oxygen supply
– Artificial respiration, may be necessary as well.
48

49. Reactivation of acetylcholinesterase:
• Pralidoxime can reactivate inhibited AChE.
• It is does not penetrate into the CNS.
• The presence of a charged group allows it to approach an
anionic site on the enzyme, where it essentially displaces the
phosphate group of the organophosphate and regenerates
the enzyme.
• If given before aging of the alkylated enzyme occurs, it can
reverse the effects of echothiophate, except for those in the
CNS.
49

50. • Pralidoxime is a weak AChE inhibitor and, at higher doses,
may cause side effects similar to other AChE inhibitors.
• In addition, it cannot overcome toxicity of reversible AChE
inhibitors (for example, physostigmine).
50

51. Cholinergic Antagonist
Cholinergic blockers
Parasympatholytics
Anticholinergic drugs
51

52. Antimuscarinic Agents
Atropine
Benztropine
Cyclopentolate
Ipratropium
Oxybutynin
Scopolamine
Tolterodine
Trihexyphenidyl
Tropicamide
Ganglionic Blockers
Mecamylamine
Neuromuscular Blockers
Non-depolarizing:
Tubocurarine
Mivacurium
Gallamine
Atracurium
Pancuronium
Vecuronium
Depolarizing:
Succinylcholine 52

53. 53

54. ANTIMUSCARINIC AGENTS
• They block:
1. muscarinic receptors, causing inhibition of all muscarinic
functions.
2. block sympathetic neurons that are cholinergic, such as
those innervating salivary and sweat glands.
54

55. Atropine
• Atropine is a tertiary amine belladonna
alkaloid with a high affinity for muscarinic
receptors.
• It binds competitively and prevents
acetylcholine (ACh) from binding to those
sites.
• Atropine acts both centrally and
peripherally.
55

56. • Duration of action:
– Systemic administration: 4 hours
– Topically in the eye: days
• Neuroeffector organs have varying sensitivity to atropine.
• The greatest inhibitory effects are on:
1. Bronchial tissue
2. Secretion of sweat and saliva.
56
Atropine

57. Therapeutic uses of Atropine:
a. Ophthalmic:
• Topical atropine exerts both mydriatic and cycloplegic effects.
– α-adrenergic drugs (Phenylephrine) are preferred for
pupillary dilation if cycloplegia is not required.
• Duration of effect on eye: 7–14 days
– Shorter-acting antimuscarinics:
• cyclopentolate and tropicamide are preferred to
produce mydriasis (6–24 hours).
57

58. • Ophthalmic precautions: may induce an acute attack of eye
pain due to sudden increases in eye pressure in individuals
with narrow-angle glaucoma.
58
Therapeutic uses of Atropine:

59. b. Antispasmodic:
– Atropine (as the active isomer, l-hyoscyamine) is used to
relax the GI tract and bladder.
c. Antidote for cholinergic agonists:
– Treatment of overdoses/termination of action of:
• Cholinesterase inhibitor (e.g. physostigmine) including
CNS effects
• Insecticides
• Some types of mushroom poisoning
59
Therapeutic uses of Atropine:

60. d. Antisecretory:
• Atropine is used as an antisecretory agent to block secretions
in the upper and lower respiratory tracts prior to surgery.
60
Therapeutic uses of Atropine:

61. Pharmacokinetics of Atropine:
– Atropine is readily absorbed
– Partially metabolized by the liver
– Eliminated primarily in urine.
– Half-life of about 4 hours.
61

62. Adverse effects of Atropine:
• Dose dependent effects:
- Peripheral effects: Dry mouth, blurred vision, tachycardia,
urinary retention, and constipation.
- CNS effects: restlessness, confusion, hallucinations, and
delirium, which may progress to depression, collapse of the
circulatory and respiratory systems, and death.
• Management of atropine toxicity: Low doses of
cholinesterase inhibitors, such as physostigmine
62

63. Scopolamine
• A tertiary amine plant alkaloid
• Its peripheral effects similar to those of atropine.
• Has greater action on the CNS (observed at therapeutic doses)
• Has a longer duration of action in comparison to those of
atropine.
63

64. Actions of scopolamine:
• Most effective as an anti–motion sickness.
• Blocks short-term memory.
• Produces sedation, but at higher doses it can produce
excitement instead.
• May produce euphoria and is susceptible to abuse.
64

65. CTZ: chemoreceptor trigger zone 65

66. Therapeutic uses of scopolamine:
• They are is limited to:
1. Prevention of motion sickness (for which it is particularly
effective)
2. blocking short-term memory (adjunct to anesthesia)
Pharmacokinetics and adverse effects:
• These aspects are similar to those of atropine.
66

67. Ipratropium and tiotropium
• They are quaternary derivatives of atropine
• Positively charged
• Administration:
 Inhalational use in pulmonary system
 do not enter the systemic circulation or the CNS
67

68. Ipratropium and tiotropium
• Clinical use: Bronchodilators:
– for maintenance treatment of bronchospasm associated
with chronic obstructive pulmonary disease (COPD).
– for treating asthma in patients who are unable to take
adrenergic agonists.
• Dosing:
– Tiotropium is administered once daily
– Ipratropium: up to four times daily.
68

69. Tropicamide and cyclopentolate
• Used as ophthalmic solutions to induce mydriasis and
cycloplegia.
• Duration of action: shorter than that of atropine:
– Tropicamide: 6 hours
– Cyclopentolate: 24 hours.
69

70. Benztropine and trihexyphenidyl
• Centrally acting antimuscarinic agents
• Previously used in the treatment of Parkinson disease.
• They have been largely replaced by newer medications such
as levodopa/carbidopa .
• They are useful adjuncts with other antiparkinsonian agents
to treat all types of parkinsonian syndromes, including
antipsychotic-induced extrapyramidal symptoms.
70

71. Darifenacin, solifenacin, tolterodine, fesoterodine, oxybutynin,
and trospium chloride
• Synthetic atropine-like drugs
• Clinical use: treatment of overactive urinary bladder disease.
• Side effects: dry mouth, constipation, and blurred vision,
which limit tolerability of these agents if used continually.
• Administration of Oxybutynin:
– is available as a transdermal system (topical patch)
– it causes less dry mouth than do oral formulations
– more widely accepted with greater patient acceptance.
71

72. Summary of therapeutic
uses for antimuscarinic
drugs
72

73. Nicotinic receptors
73

74. Nicotinic receptors
• Found in autonomic ganglions,
adrenal medulla, neuromuscular
junction and CNS
• Ligand-gated ion (Na+) channel.
Ach binds to the α subunits
74

75. Nicotinic receptors
• Blocking gaglionic AChR blocks all
autonomic outflow.
• These agents lack selectivity and
are now used mostly in research
laboratories
• These blocking agents include:
Hexamethonium
Tetraethylammonium
Mecamylamine
Trimethaphan
75

76. Neuromuscular-blocking drugs
76

77. • They block cholinergic transmission between motor nerve
endings and the nicotinic receptors on the neuromuscular
endplate of skeletal muscle.
• Structural analogs of ACh, act either as:
– Competitive antagonists (nondepolarizing type) or
– Agonists (depolarizing type) at the receptors on the
endplate of the NMJ.
77
Neuromuscular-blocking drugs

78. Clinical uses of neuromuscular-blocking drugs
• They are skeletal muscle relaxants.
– Such agents are also useful in:
• Orthopedic surgery
• Facilitating tracheal intubation.
– The neuromuscular-blocking agents have significantly
increased the safety of anesthesia, because less anesthetic
is required to produce muscle relaxation, allowing patients
to recover quickly and completely after surgery.
78

79. A. Competitive antagonists (nondepolarizing type) NM
blocker
– Tubocurarine
– Atracurium
– Pancuronium
– Vecuronium
– Gallamine
Neuromuscular-blocking drugs
79

80. Nondepolarizing (competitive) blockers
• Curare
– First drug used in blocking the
skeletal NMJ.
– Used by native South American
hunters of the Amazon region to
paralyze prey. Strychnos toxifera
80

81. Tubocurarine: the prototype
• in clinical practice in the early 1940s.
• it has been largely replaced by other agents because of its
adverse side effects.
81

82. Mechanism of action Nondepolarizing (competitive)
blockers:
a. At low doses:
• Interact with the nicotinic receptors
to prevent the binding of ACh.
• They prevent depolarization of the
muscle cell membrane and inhibit
muscular contraction.
• They are called competitive blockers.
82

83. Reversing the action Nondepolarizing (competitive)
blockers:
• Administration of cholinesterase inhibitors (e.g.
Physostigmine)
• Anesthesiologists often employ this strategy to shorten the
duration of the neuromuscular blockade.
83

84. b. At high doses:
• Can block the ion channels of the endplate.
• This leads to further weakening of neuromuscular
transmission, thereby reducing the ability of AChE inhibitors
to reverse the actions of the non depolarizing muscle
relaxants.
84
Mechanism of action Nondepolarizing (competitive)
blockers:

85. • Not all muscles are equally sensitive to blockade by
competitive blockers
i. Small, rapidly contracting muscles of the face and eye
are most susceptible and are paralyzed first, followed by
the fingers.
ii. The limbs, neck, and trunk muscles are paralyzed.
iii. Next, the intercostal muscles are affected
iv. Lastly, the diaphragm muscles are paralyzed.
• The muscles recover in the reverse manner.
85
Mechanism of action Nondepolarizing (competitive)
blockers:

86. • Those agents release histamine (for example, atracurium) can
cause:
1. Hypotention
2. Flushing
3. Bronchoconstriction
86
Mechanism of action Nondepolarizing (competitive)
blockers:

87. a) Adjunct drugs in anesthesia during surgery;
would act as skeletal muscle relaxants.
b) During orthopedic surgery (for example, fracture alignment
and dislocation corrections).
c) Used to facilitate intubation
87
Therapeutic uses of Nondepolarizing (competitive)
blockers:

88. a patient is intubated and connected to an
anesthesia breathing machine
88

89. 89

90. Atracurium
• As potent as curare (1.5)
• Has intermediate duration of action (30 min).
• Eliminated by non enzymatic chemical degradation in plasma
(Spontaneous hydrolysis at body pH).
• The drug of choice in liver failure & kidney failure.
• Liberates histamine (Transient hypotension ).
• No effect on muscarinic receptor nor ganglia .
90

91. Mivacurium
• Chemically related to atracurium
• Metabolized by pseudocholinesterases.
• Fast onset of action
• Short duration of action (15 min).
• Transient hypotension (histamine release).
• Longer duration in patient with liver disease or genetic
cholinesterase deficiency.
91

92. Depolarizing agents
Succinylcholine (Suxamethonium)
• They depolarize the plasma membrane of the muscle fiber,
similar to the action of ACh.
• Succinylcholine is the only depolarizing muscle relaxant in use
today.
• These agents are more resistant to degradation by AChE, and
can thus more persistently depolarize the muscle fibers.
92

93. Mechanism of action of Succinylcholine:
• Causes the opening of the sodium channel associated with
the nicotinic receptors, which results in depolarization of the
receptor.
• This leads to a transient twitching of the muscle
(fasciculations).
• It remains attached to the receptor for a relatively longer time
and providing constant stimulation of the receptor.
93

94. • Sustained depolarization of post-junctional membrane
(results in inactivation of Na channels), causes the
postjunctional membrane to become unresponsive to ACh
released by motor neurons.
• This is referred to as “Phase I block” & produces a
characteristic reduction in contractile response.
94
Mechanism of action of Succinylcholine:

95. • In less than a minute after IV administration a flaccid paralysis
develops due to the development of a desensitized state
• The membrane becomes repolarized, but insensitive to ACh
(due to receptor desensitization).
• This is referred to as “Phase II block”
95
Mechanism of action of Succinylcholine:

96. • Initially produces:
– brief muscle fasciculations
– a ganglionic block
• At high doses, has weak histamine releasing action.
• The duration of action of succinylcholine is extremely short:
– rapidly broken down by plasma pseudocholinesterase.
96
Action of Succinylcholine:

97. Therapeutic uses of Succinylcholine:
a) Endotracheal intubation: during the induction of anesthesia
b) To control convulsion during electroconvulsive shock
treatment.
97

98. • Succinylcholine is injected intravenously.
• Onset of action: 1 minute
• Its brief duration of action (5-10 minutes) results from:
– Redistribution
– rapid hydrolysis by pseudocholinesterase.
98
Pharmacokinetics uses of Succinylcholine:

99. Adverse effects of succinylcholine:
a. Malignant Hyperthermia: When used with the anesthetic
drug halothane
• Symptoms: muscular rigidity, metabolic acidosis, tachycardia,
and hyperpyrexia) in genetically susceptible people.
• Treatment:
1. Stop drug
2. IV Dantrolene
3. rapidly cooling of the patient with ice
99

100. 100

101. b. Apnea: When administered to a patient who is:
– genetically deficient in plasma cholinesterase or
– who has an atypical form of the enzyme
• can lead to prolonged apnea due to paralysis of the
diaphragm.
101
Adverse effects of succinylcholine:

102. c. Hyperkalemia:
• Succinylcholine increases potassium release from intracellular
stores.
• While the receptor is open, continued flow of potassium ions
into the extracellular fluid.
102
Adverse effects of succinylcholine:

103. Skeletal muscle relaxants, types:
1. Peripherally acting (Neuromuscular blockers).
2. Centrally-acting
– They include:
1. Diazepam, which binds at γ-aminobutyric acid
(GABA_A) receptors
2. Baclofen, which probably acts at GABA_B receptors in
the CNS.
3. Direct-acting
– Dantrolene: acts directly on muscles by interfering with
the release of calcium from the sarcoplasmic reticulum 103