BIOP211
www.endeavour.edu.au
Session 10
Pharmacology:
Drugs Affecting the
Peripheral Nervous
System
Department of Bioscience
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BIOP211 - PHARMACOLOGYSESSION OUTLINE: Drugs acting in the Peripheral NS
o Neurotransmitters and their agonists and antagonists in
the Peripheral Nervous System.
o Review neurotransmitters involved in both the
Sympathetic Nervous System and Parasympathetic
Nervous System.
o Anti-muscarinic drugs and their effects.
o Adrenergic and anti-adrenergic drugs and their effects.
o Review the Somatic Nervous System and the
Neuromuscular Junction.
o Acetylcholinesterase activity and the drugs used to block
this enzyme (AChase Inhibitors).
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The Nervous System
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Autonomic Nervous System
o The autonomic nervous system (ANS) is responsible
for regulation of the internal viscera such as the heart,
blood vessels, digestive organs, kidneys and
reproductive organs.
o The ANS regulates homeostasis (maintains an optimal
internal environment).
o It cannot function independently of the CNS.
o ANS functions are not under direct conscious control
(e.g. regulation of heartbeat).
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The Autonomic
Nervous System
sub divisions The ANS has 3 subdivisions:
Parasympathetic NS Conserves energy and restores body
resources (e.g. reduces heart rate,
and increases GI activity).
Sympathetic NS Dominates body in stress and
emergency. Responsible for “fight or
flight” response (e.g. ↑ in blood
[sugar], heart rate and BP).
Enteric NS (ENS)
Functions independently of CNS.
(Controls motility, secretion,
microcirculation).
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Neurotransmitters
o To date, over 50 different endogenous chemicals have
been identified as neurotransmitters (or presumed
neurotransmitters).
o Key neurotransmitters include:
• Acetylcholine (ACh).
• Noradrenaline (NA).
• Adrenaline (A).
o Others include dopamine, 5-HT (serotonin), histamine,
substance P, endorphins, enkephalins.
o ACh and NA are the principle neurotransmitters in the
autonomic nervous system (ANS).
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Basic Principles - ACho Nerve fibres that release acetylcholine (ACh) are said
to be cholinergic.
o ACh is the neurotransmitter released from:
• Preganglionic neurons in both P-SNS and SNS.
• Postganglionic parasympathetic nerve fibres.
• Sympathetic postganglionic neurons that innervate
sweat glands.
o ACh is the key neurotransmitter involved in
parasympathetic NS function and activity
(conservation of energy / restoration).
o ACh activates 2 types of receptors:
• Muscarinic [M1 (neural), M2 (cardiac & presynaptic),
M3 (glandular or smooth muscle type)].
• Nicotinic [Nn (neuronal) , Nm (muscle)].
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Basic Principles - NAo Nerve fibres that release noradrenaline (NA) (or are
sensitive to adrenaline) are said to be adrenergic.
o NA acts as the neurotransmitter between sympathetic
postganglionic nerves and the organs they innervate.
o NA and A are the key neurotransmitters involved in
the sympathetic NS and functions (stress response /
“fight-flight”.
o There are two types of adrenergic receptors:
• Alpha (1 and 2).
• Beta (1, 2 and 3).
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Cholinergic
transmission
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Noradrenaline and adrenergic
transmission
o The term catecholamine refers to a group of
chemically related compounds:
• Noradrenaline (NA).
• Adrenaline (A).
• Dopamine (DA) – precursor to NA and A; also has a
principle role as a neurotransmitter in the brain. It is
important in diseases such as Parkinson’s and
schizophrenia.
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Adrenergic Transmission
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Adrenergic Receptors – α1 & α2
o There are two types of adrenergic receptors → alpha (α)
and beta (β):
o Alpha 1 (α1) receptors - situated on the post synaptic
membrane; adrenergic receptor stimulation leads to:
• vasoconstriction of peripheral blood vessels.
• dilation (contraction) of pupil.
• increased contractility of heart (inotropic effect).
o Alpha 2 (α2) receptors are located on pre-synaptic nerve
terminals (and also on liver, platelets and blood vessel
smooth muscle cells; adrenergic stimulation leads to:
• Inhibition of transmitter release.
• Aggregation of platelets.
• Contraction of smooth muscle.
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Adrenergic Receptors, Beta (β)1 & 2
o Beta 1 (β1) receptors are located primarily in the heart.
Receptor stimulation leads to:
• Increased heart rate (chronotropic effect).
• Increased contractility of heart (inotropic effect).
o Beta 2 (β2) receptors are located in the smooth muscle in
bronchioles, blood vessels and other visceral organs.
Receptor stimulation leads to:
• Relaxation of uterus.
• Glycogenolysis (breakdown of glycogen).
• Dilation of bronchial smooth muscle.
o Beta 3 (β3) receptors are localized to adipose tissue.
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NA and A
o Noradrenaline excites mainly Alpha (α) receptors, butexcites Beta receptors to slight extent as well.
o Adrenaline excites Alpha (α) and Beta (β) receptors equally.
o The extent to which NA and A will excite various organs isdependent on the relative numbers of alpha (α) and beta (β)receptors that the organ contains (e.g. the heart containsmainly β1 receptors – affected mostly by adrenaline.
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Drugs at Cholinergic receptors
o Drugs that antagonise or block the action of
acetylcholine, ACh, at the muscarinic receptor sites (M)
are referred to as: Muscarinic receptor antagonists or
Antimuscarinic drugs or Anticholinergic drugs.
o Use of these drugs means acetylcholine cannot bind to
the muscarinic receptor site and thus fails to produce a
cholinergic effect.
o parasympathetic system of the autonomic nervous
system use acetylcholine as the main neurotransmitter,
Anticholinergic action = anti-parasympathetic response
(= parasympatholytic).
o Cholinergic action = increased parasympathetic
response.
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Cholinergic Drugso Drugs that mimic the action of ACh on the
Parasympathetic Nervous System (PSNS) are also
known as muscarinic receptor agonists or
parasympathomimetic drugs.
o Only three of these are used clinically
• Bethanechol (used systemically for urinary and
gastro-intestinal symptoms – promotes micturition
and gastric motility).
• Carbachol (eye drops or intraocular injection used in
glaucoma).
• Pilocarpine (eyedrops used in glaucoma).
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Anticholinergic drugs – anti-
muscarinicso The best known muscarinic antagonists are atropine and
hyoscine.
o Atropa belladonna (Deadly nightshade) contains atropine.
o Hyoscyamus niger (henbane) and Datura stramonium
(jimsonweed) contain hyoscine.
1024px-Atropa_belladonna_002.JPG, n.d. Atropa
belladonna, Solanacae..viewed
http://insertmedia.office.microsoft.com
Invasive.org, n.d.
Blackhenbane -
Herblore.viewed
http://insertmedia.off
ice.microsoft.com
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Atropineo Prototype muscarinic antagonist (very little action on nicotinic
receptors).
o Used for > 50 years.
o Often the adverse effects of anticholinergic drugs are referred to as“atropine-like” adverse effects.
Atropine can produce a wide range of pharmacological effects becauseof the widespread distribution of parasympathetic cholinergic nerves inthe body:
o Eyes: pupil dilation (mydriasis = Belladonna, beautiful lady).
o Skin and mucous membranes: inhibits secretions.
o Respiratory system: relaxes muscle of the bronchial tract.
o Cardiovascular system: low doses decreases HR.
o GIT: high doses inhibits GI motility.
o Urinary tract: relaxes smooth muscle & ↑ sphincter constriction.
o CNS: excitement and mania.
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Hyoscine hydrobromide
o Hyoscine is a muscarinic receptor antagonist, similar in
chemical structure to atropine.
o The peripheral effects are similar to atropine but
because it is rapidly absorbed through the BBB, it has
marked effects on the CNS.
o Indications: Used for motion sickness (prevents nausea
and vomiting), and as an adjunct medication with general
anaesthesia to reduce respiratory tract secretions.
o Adverse effects: Causes drowsiness, euphoria,
memory loss, relaxation, sleep, relief of fear and
depresses CNS. Does not increase blood pressure or
respiration.
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ANTICHOLINERGIC ADVERSE EFFECTS
(Seen with many drugs including atropine, antihistamines,
tricyclic and tetracyclic antidepressants)
o Tachycardia
o Heart palpitations
o Decreased bronchial
secretions
o Antispasmodic effects
o Mydriasis (expanding
pupil) and blurred vision
o Dry mouth
o Urinary retention
o Male impotence
o Decreased gut motility
(leading to constipation)
o Dizziness
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Anticholinergic Drugs, C/I and
Drug-drug interactions
Drug Interactions
o Additive effects with TriCyclic Antidepressants (TCAs),
some antihistamines (promethazine).
o Impair absorption of other drugs (due to reduction in
gastric motility).
Warnings & Contraindications
o Many C/I including myasthenia gravis, severe cardiac
disease, GI obstructive disease, narrow angle glaucoma.
Caution in Down’s syndrome, elderly, hepatic and renal
disease.
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Sub-classes of Adrenergic Drugs
and anti-adrenergic drugs
1. Direct-acting sympathomimetic drugs (agonists)
• Mimics the effects of NA or A.
2. Indirect-acting sympathomimetic drugs
• Facilitate the release of NA or block the uptake of NA
into nerve terminals.
3. Adrenoreceptor antagonists (blockers) /sympatholytic
drugs
• Block action of sympathetic nervous system.
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1. Direct-acting Sympathomimetic
Drugs
o Sympathomimetic drugs are those that mimic the effect
of NA (noradrenaline) on sympathetic effector organs.
o Use leads to a ‘sympathetic response’ (fight/flight) such
as an increase in cardiac output, vasoconstriction of
arterioles and veins, regulation of body temperature,
bronchial dilation.
o Naturally occurring catecholamines (adrenaline,
noradrenaline and dopamine) may be used as drug
therapies, as well as synthetic catecholamines (e.g.
isoprenaline and others).
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1. Direct-acting Sympathomimetic
Drugs (adrenoceptor agonists)
o Responses mediated by and stimulation:
o -Stimulation leads to:
• Vasoconstriction in peripheral blood vessels leading
to increased blood pressure.
• pupil dilation.
• relaxation of the gut.
o -Stimulation leads to:
• Increased heart rate and contractility.
• Vasodilation of skeletal muscle arterioles.
• Bronchial relaxation and uterine relaxation.
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Control of NA
release
Alpha2 (α2) receptors are
found on presynaptic nerve
terminals, and post synaptic
vascular and smooth muscle
cells. The presynaptic alpha2
(α2) receptors control the
amount of NA released per
nerve impulse (high
concentration prevents release
of more NA).
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1. Adrenaline (as drug therapy)
o Stimulates both and receptors (dose dependent butat therapeutic doses primarily receptors of the heart,smooth muscle of the bronchi and the blood vessels.
o Positive inotropic effects (increase in myocardialcontraction).
o Positive chronotropic effect (increased cardiac rate).
o Dromotropic effect (improved atrio-ventricularconduction).
o Vascular effects are dose dependent but low dosesdecrease total peripheral resistance (lower bloodpressure) and high doses increase bp.
o CNS effects (restlessness, tremor, anxiety).
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1. Other effects of Adrenaline
o Smooth muscle effects (relaxes but constricts sphincter
e.g. delay in desire to void urinary bladder).
o Respiratory effects, powerful bronchodilator (hence
indications later in allergic responses).
o Metabolic effects i.e. (increased availability of fuels,
glucose and free fatty acids in blood), increases O2
consumption.
o Effects on skeletal muscle (vasodilation).
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1. Indications - Adrenaline
o Emergency treatment of acute anaphylactic shock and
severe allergic reactions.
o As an adjunct to local anaesthetics.
o As a haemostatic agent to control superficial bleeding.
o In ocular surgery to prevent bleeding.
o To treat cardiac arrest.
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1. Adrenaline – ADR and Drug Drug
Interactionso Nervousness, insomnia, tachycardia, tremors, sweating,
hypertension, nausea, vomiting. High doses may cause
ventricular arrhythmias.
o Contraindications: include Diabetes mellitus,
Hypertension, Ischaemic heart disease, Hyperthyroidism,
Parkinson's disease.
o Drug Interactions include
o Anaesthetics, β-blockers, Digoxin, Oxytocics.
o TriCyclic Antidepressants (TCA), monoamine oxidase
inhibitors (MAOI) cocaine (potentiate the effect of
adrenaline).
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2. Noradrenaline
o NA has a high affinity for receptors, producingvasoconstriction in skin and mucous membranes aswell as blood vessels in visceral organs(predominantly receptors ).
o Restores arterial blood pressure in acutehypotensive states.
o Also used as adjunct in cardiac arrest (IVadministration, as inactivated in GIT).
o Adverse reactions: include anxiety, dizziness,tremor.
o Contraindications: e.g. use with caution inatherosclerosis, hypoxia.
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3. Isoprenalineo synthetic catecholamine and non-selective -
adrenoceptor agonist (stimulates 1 and 2 receptors).
o 1 receptors – leads to ↑ force of myocardial contraction
and heart rate.
o β2 receptors – leads to relaxation of smooth muscle of
bronchi.
o Indications: cardiac stimulant (adjunct e.g. in septic
shock, hypovolaemic states).
o Adverse reactions: (see adrenaline).
o Cautioned use in elderly, diabetics and in
hyperthyroidism.
o Contraindications: e.g.Tachycardia, myocardial infarct.
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4. Dopamineo Dopamine is an immediate precursor to A and NA.
o It stimulates dopaminergic receptors, 1 receptors, and inhigh doses, 1 and 2 receptors.
o Actions of dopamine are dose dependent and complex.
o At low to moderate doses.
• Direct effect on 1 receptors and stimulates releaseof NA.
• Increased heart rate and stroke volume (cardiacoutput, CO).
o Indications – e.g. used in the treatment of circulatoryshock, Congestive heart failure (CHF).
o Adverse reactions: can include Headaches, nausea,vomiting, angina, ↓BP. Less frequently: hypertension.
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Summary 1. Direct Acting
Sympathomimeticso Agonists at α1 α2 β1 β2 receptors.
o Adverse effects explained by non-selective effects at
other receptor types and subtypes.
o Adrenaline – dose related effects, α1 α2 β1 β2 ,indications
for asthma, local haemostasis, acute anaphylactic shock,
Open Angle Glaucoma (OAG), cardiac arrest.
o Isoprenaline – synthetic catecholamine.
o Noradrenaline, dose related effect kidney & other visceral
organs, α receptors stimulated at high dose; indications,
shock.
o Dopamine, dose related effect, D1 & direct & indirect
effects on β 1, high dose α1 & α2, indications, circulatory
shock, CCF.
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2. Indirect-Acting Sympathomimetics
o This group of drugs trigger the release of noradrenaline
and adrenaline from their storage sites.
o These neurotransmitters then activate and receptors
o Agents in this class include:
• Ephedrine (used in cold and flu tabs, also some diet
pills).
• Pseudoephedrine (in cold and flu tabs).
• Amphetamines.
• Metaraminol.
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3. Adrenoreceptor Antagonists
o Adrenoreceptor antagonists compete with
catecholamines at the receptor and inhibit (of block)
sympathetic stimulation and effect.
o These are generally classes according to which receptor
is blocked ie
• -Blockers (or adrenoceptor antagonists).
• -Blockers (or adrenoceptor antagonists).
o Drugs in this class may be selective or non-selective for
a specific receptor.
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-Blockers
- adrenoreceptor antagonists (blockers) compete with
catecholamines (A and NA) at the -receptor sites and
inhibit sympathetic stimulation.
The main groups of drugs are:
o 1 -Selective antagonists (e.g. prazosin, terazosin,
doxazosin).
o Non-selective (1- 2) antagonists (e.g.
phenoxybenzamine, labetalol).
o Ergot alkaloids, which are partial –adrenergic blockers
(used to treat migraine).
© Endeavour College of Natural Health www.endeavour.edu.au 37
1-Selective antagonist
o Examples: Prazosin, terazosin, doxazocin, tamsulosin.
o Indications: - Used for treatment of hypertension and
symptomatic relief of urinary obstruction in benign prostatic
hyperplasia (BPH).
o Mechanism of Action:
• Selective blockade of postsynaptic 1 receptors results in ↓
in peripheral vascular resistance due to inhibition of
catecholamine-induced vasoconstriction. Use only leads
to a minor increase in heart rate because these drugs
have low 2-adrenoceptor activity.
• Reduced resistance to urinary flow in neck of bladder due
to blockade of receptors on the smooth muscle.
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Adrenoreceptor antagonists
o Also known as blockers.
o May be selective or non-selective (for 1 and/or 2
receptors).
o The prototype of blockers is propranolol which is non-
selective (blocks 1 and 2 receptors). It is thus also
associated with a higher incidence of adverse effects
(action is indiscriminate).
o At high doses, 1 selective blockers will also block 2
receptors (leading to unwanted effects).
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β-Blockers
o Mechanism of Action: -blockers competitively block
receptors in heart etc blocking the actions of
catecholamines (A and NA) at these sites (mechanism of
ADR: Cardiac muscle contains principally 1
receptors and smooth muscle sites e.g. airways contain
mainly 2 receptor sites).
• Cardiac effects (anti-anginal, decrease all heart
parameters).
• Metabolic effects (if non-selective effects, blocks
responses to hypoglycaemia, increase triglycerides and
decrease HDL cholesterol in serum).
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-Blockers - Indications
o Hypertension (Usually 1-selective blockers (also knownas cardioselective) e.g. atenolol, betaxolol, esmolol.
o Angina pectoris.
o Tremors and tachycardia associated withhyperthyroidism and anxiety.
o Myocardial infarction (MI).
o Phaeochromocytoma (rare catecholamine-secretingtumour of adrenal medulla).
o Glaucoma.
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-Blockers - Safety
Adverse effects
o Insomnia, nightmares, depression, nausea, diarrhoea,
dizziness, fatigue, hypotension, heart failure, heart block,
bradycardia, bronchospasm and shortness of breath,
(SOB).
Contraindications:
o Heart block, bradycardia, cardiogenic shock, asthma,
chronic obstructive airway disease (COAD) & severe
hypotension.
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Sites of Action
of Drugs
affecting
Noradrenergic
transmission
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Somatic Nervous System
o The somatic nervous system is a division of the
peripheral nervous system (PNS) that co-ordinates
consciously controlled functions, including movement
(gross and precise), posture and respiration.
o Drugs may be used to block neuromuscular
transmission e.g. As an adjunct to anaesthesia, leading
to muscle relaxation.
o In clinical practice, drugs known as anticholinesterase
agents are used to reverse this neuromuscular blockade.
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Somatic Nerve Transmission - NMJ
o When a nerve action potential arrives at the
neuromuscular junction (NMJ), acetylcholine (ACh) is
released which diffuses across the synaptic cleft to act
on postsynaptic nicotinic receptors on the motor end-
plate of the muscle fibre, leading to muscular
contraction.
o The action of ACh is rapidly terminated by the enzyme
acetylcholinesterase.
© Endeavour College of Natural Health www.endeavour.edu.au 45
Somatic Nerve Transmission
o The release and metabolism of ACh occurs according to
the same mechanisms described for the Autonomic
PNS.
o The difference is that in the somatic NS, ACh acts on
postsynaptic nicotinic receptors, whereas in the
Autonomic PNS it acts on postsynaptic muscarinic
receptors.
o Thus nicotinic receptors mediate the effect of ACh on
skeletal muscle.
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Neuromuscular
Junction, NMJ
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Neuromuscular Blocking Drugs
o Many sites where drugs and toxins can interrupt
neuromuscular transmission.
• Blockade of action potential generation in the motor
neuron.
• Inhibition of release of ACh.
• Blockade of postsynaptic receptors.
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Neuromuscular Blocking Drugs There are two types of neuromuscular blocking drugs:
1. Non-depolarising (competitive) drugs that
competitively block the action of ACh at post and
presynaptic nicotinic receptors, which blocks the normal
feedback loop that increases the release of ACh under
conditions of enhanced stimulation. E.g.. Tubocurarine
(does not cross BBB nor placenta but release histamine
and rare ADR).
2. Depolarising drugs (nicotinic agonists) maintain the
depolarised state of the motor end-plate, thus
preventing transmission of another muscle action
potential. E.g.. Suxamethonium. For endotracheal
intubation and muscle relaxation for short procedures.
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Anticholinesterases or AChE Inhibitors
o The enzyme acetylcholinesterase (AChE) hydrolyses
(breaks down) ACh, forming choline and acetate.
o There is a class of drugs known as anticholinesterases
or AChE inhibitors (act to stop hydrolysis of ACh).
o These drugs are used to reverse the effects of the
neuromuscular blocking drugs (non-depolarising) after
anaesthesia.
o They also have other clinical uses for some medical
conditions such as in glaucoma, Alzheimer’s disease
and myasthenia gravis.
o Some organophosphate pesticides contain irreversible
anticholinesterase agents (toxicity is a result of
accumulation of ACh and excess stimulation of the
somatic, autonomic and central nervous systems).
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Tutorial / Forum Discussion SN10
Drugs Affecting the Peripheral NSDiscuss these medications acting in the Peripheral Nervous System, PNS. 10 marks for (i) examples (for adrenaline
hormone, give other catecholamines that are neurotransmitters but also used as drugs) (ii) indications (iii) mechanism
of action (iv) efficacy and limitations or cautions / contra-indications (v) adverse effects. Mark your own answer using
the Pharmacology text or online resources. Alternatively, peer review each other’s answers, allocating 10 marks per
drug class
o Adrenergic hormones as drugs, e.g. adrenaline (called epinephrine
in the USA)
o Synthetic adrenergic agents e.g. isoprenaline
o Indirect acting sympathomimetic agents
o Alpha-selective antagonists
o Beta blockers
o Neuromuscular blocking drugs
o Anticholinesterase drugs (also known as AChEase Inhibitors)
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Bibliography
o Bryant B, Knights K. 2007. Pharmacology for health
professionals 3nd Edition. Mosby Elsevier
o Tortora, G.J. and Derrickson, B. 2013. Principles of
anatomy and physiology. 14th edition Wiley, USA.
© Endeavour College of Natural Health www.endeavour.edu.au 52
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