Autonomic nervous system pharmacology

Pharmacology of
autonomous nervous
system
By:- Getahun D (B.pharm, MSc St.)

Objective
At the end of the chapter , you are expected to describe
the following points:
The physiological function of PSNS and SNS
The location of ACH and NE
Discuss Parasympathomimetic and parasympatholytic
agents
Describe sympathomimetic and sympatholytic drugs
Tuesday, January 28, 2020 2

Review of anatomy & physiology of
the autonomic nervous system
3
Carry signals
away from the
brain and spinal
cord to the
peripheral tissues
Bring information from
the periphery to the CNS
1/28/2020

ANS…..
 It is largely autonomous (independent) in that its
activities are not under direct conscious control.
 It functions to innervate smooth muscle,
cardiac muscle and exocrine glands.
 It is concerned primarily with visceral functions
such as cardiac output, blood flow to various
organs, and digestion, which are necessary
for life.
41/28/2020

 Differences between Autonomic and Somatic
Nervous system
 The effector cells innervated by the somatic
nervous system are skeletal muscle cells.
 It is a voluntary system; it is largely concerned
with consciously controlled functions such as
movement, respiration, and posture.
 ANS is classified anatomically into two major
portions: the sympathetic (thoracolumbar)
division and the parasympathetic (craniosacral)
division.
 Both divisions originate in nuclei within the CNS
and give rise to preganglionic efferent fibers that
exit from the brain stem or spinal cord and
terminate in motor ganglia 51/28/2020

Autonomic Nervous System
(ANS)…
• Parasympathetic vs. sympathetic systems
A. Parasympathetic system
Most preganglionic fibers originate in the midbrain or
M. oblongata of the brain and few from sacral portion
of CNS.
Ganglia are found close to or within innervated organ
It controls many day to day functions such as flow of
saliva, peristalsis, constriction of pupil and
accommodation of near vision.
61/28/2020

B. Sympathetic system
Preganglionic fibers begin in thoracic and lumbar
columns of spinal cord
Ganglia are found far away from innervated organ.
Its stimulation prepares the body for Fight, Flight
and Fright

Employ three different transmitters namely ACh, NA & A.
1/28/2020 11

Difference between PSNS and SNS
Parasympathetic Nervous
System
This system is concerned with
the conservation of the body
processes.
Its main neurotransmitter is
acetylcholine.
Its receptors are muscarinic,
nicotinic
Cranio-sacral
Sympathetic Nervous System
This nervous system is
designed to cope with
emergency situations.
Its neurotransmitters are
epinephrine and norepi.
Its receptors are the α and
β
Thoraco-lumbar

The ANS has three principal functions:
1. Regulation of the heart
2. Regulation of the secretory glands
- salivary
- gastric
- sweat and bronchial glands
3. Regulation of smooth muscles,
- muscles of bronchi
- muscles of blood vessels
- muscles of urogenital
- muscles of GIT
1/28/2020 13

Major function of PsNs;
 Specifically, stimulation of appropriate PsN will cause:
1. slowing of the heart
2. increased gastric secretion
3. emptying of the bowel
4. emptying of the bladder
5. focusing of the eye for near vision
6. constriction of the pupil
 Agents that work by altering parasympathetic nervous
system function are used primarily for their impact
upon-
 the gastrointestinal tract
 the bladder
 the eye
1/28/2020 14

Major functions of SNS
 The main functions of the sympathetic nervous
system are:
A. Regulation of CVS
B. Regulation of body temperature
C. Initiation of "fight" or "flight" reaction.
 Characteristic features:
a) Shunting of blood away from the skin and
visceral into skeletal muscles.
b) Dilation of the bronchi to improve
oxygenation
c) Dilation of the pupil
d) Mobilization of stored energy1/28/2020 15

Parasympathomimetics agents
Cholinergic drugs or cholinomimetics
They stimulate parasympathetic nervous system in same
manner as does acetylcholine
They may stimulate cholinergic receptors directly or
They slow acetylcholine metabolism at synapses
They are useful in treating Alzheimer's disease, myasthenia
gravis and to treatment of atony of the smooth muscle
(GIT, urinary system)

Acetylcholine
 Acetylcholine is released at preganglionic fibers of both the
sympathetic and parasympathetic nervous system
 Also released from postganglionic sympathetic neurons that
innervate the sweat glands and from motor neurons that innervate
the skeletal muscles
 It is a quaternary ammonium compound so cannot penetrate the
membrane
 Have limited therapeutic importance, because of multiplicity of
actions and rapid inactivation by ACHase.
 Used only to produce miosis in ocular surgery

Life cycle of acetylcholine

Cholinergic receptors

Cholinergic drugs are classified into two types :
A.Direct acting: They act by binding directly to
cholinoceptors
a. Endogenous choline esters eg: carbachol, methacholine
and bethanechol
b. Naturally occurring alkaloids eg: nicotine and pilocarpine
B. Indirect acting:They act through inhibition of
acetylcholinesterase enzyme, so increases acetylcholine
level in the synapse
I. Reversible
II. Irreversible

Direct acting cholinergics
Pilocarpine
 lipid soluble
 It has muscarinic activity only
 When applied locally to cornea produces rapid miosis
and contraction of ciliary muscle produces of spasm
of accommodation and vision is fixed at particular
distance making it impossible to focus for far
situated objects
 Used in glaucoma (outflow obstruction of aqueous
humour) since it facilitate the drainage.

Indirect acting cholinergic agonists
Mechanism of action
• They act through
inhibition of enzyme, so
increases acetylcholine
level in the synapse

Classification
Reversible
Neostigmine
Physostigmine
Pyridostigmine
Edrophonium
Tacrine
Danopezil
Irreversible
Ecothiophate
Malathion
Parathion
Sarin

Physostigmine
 It is a tertiary amine (uncharged)
Completely absorbed from the GIT
Highly distributed throughout the body including BBB
 It is intermediate-acting (2-4hr duration of action)
 It stimulates muscarinic and nicotinic receptors
 Indications: Glaucoma (closed) ,Atony (intestinal and
bladder)
 Treatment of overdoses of drugs with anticholinergic
actions(TCAs or atropine)

Neostigmine
 It is quaternary ammonium
Poorly absorbed after oral administration; nevertheless, is
orally active if larger doses are employed.
Poorly distributed throughout the body
It cannot pass the blood brain barrier
 Has a moderate duration of action, usually 30 min to 2hr
 Unlike physostigmine, it has additionally a direct nicotinic
action on skeletal muscle
 Indications: atony (intestinal and bladder),for reversal of
effect of muscle relaxants(Comp. NMBs) and for myasthenia
gravis

Irreversible agents:
Have prolonged and pronounced effects on
cholinergic systems.
Although several of these compounds are used
topically to treat glaucoma, most are insecticides
and are potent war gases.
1. Parathion and Malathion
Are common insecticides used in agriculture
Parathion itself is prodrug.
2. Sarin and Soman
Are potent anti-cholinesterase war gases
Unfortunately, their actions are not reversed by
the enzyme reactivators.
261/28/2020

Clinical uses of the cholinomimetics
A. Eye
Glaucoma (open angle, closed angle)
Decrease IOP by increasing outflow of aqueous humor.
٠Pilocarpine and carbachol
٠ long acting [ecothiopate] if control of IOP can not be
achieved
B. GIT &Urinary tract
 Postoperative ileus (atony/paralysis of the stomach or bowl
following surgical manipulation) & congenital megacolon
 Urinary retention (postoperative/postpartum)
Bethanehol - GIT problems (10-25mg, 3-4 times/day PO)
- Urinary retention 5mg sc
Neostigmine- paralytic ileus /atony of bladder (0.5 –1mg sc)
 Xerostomia (Pilocarpine, Bethanechol)
271/28/2020

C. Neuromuscular junction
Myasthenia gravis: autoimmune process causes
production of antibody that decrease the number of
functional nicotinic receptors on the postjunctional
endplates.
• Direct acting cholinocepor (not effective)
• Edrophonium (2mg) for diagnosis
• Neostigmine and pyridostigmine is used to treat
chronic long term myasthenia gravis
D. Heart
Short acting cholinesterase – paroxysmal
supraventricular tachycardia
E. Antimuscarinic drug intoxication
 Atropine, TCA have antimuscarinic effect
 Physostigmine is better since it can cross BBB
281/28/2020

Toxicity
A. Direct acting muscarinic stimulant
 Nausea, vomiting, diarrhea, salivation, sweating,
cutaneous vasodilation, bronchial constriction
Certain mushrooms contain muscarinic alkaloid →
typical signs of muscarinic excess.
[Treatment: atropine 1-2mg]
B. Direct acting nicotinic stimulants (nicotine)
CNS stimulation (convulsion, coma, & respiratory
arrest)
Skeletal muscle depolarization blockage &
respiratory paralysis
Hypertension
291/28/2020

Cholinesterase inhibitors in CNS
Tacrine, Rivastigmine, and Donepezil
The drugs readily enter the CNS
They used as possible remedies for the loss of cognitive
function in patients of Alzheimer's disease (a deficiency of
cholinergic neurons in the CNS)
Only to delay the progression of the disease but none can
stop its progression
Gastrointestinal distress is their primary adverse effect

Contraindications to the use of cholinomimetics
Bronchial asthma:- induce bronchial constriction and
increase bronchial secretions
Hyperthyroidism:- danger of inducing AFi
Peptic ulcer disease:- increase in gastric acid secretion
Coronary insufficiency:- hypotension produced will further
compromise coronary blood flow
Mechanical intestinal and urinary outlet obstruction

Anticholinergics

Antimuscarinics
Uses of antimuscarinics:
For the treatment of overdoses of acetyl cholinesterase
inhibitor insecticides
Some types of mushroom poisoning (certain mushrooms
contain cholinergic substances that block cholinesterase).
Chronic obstructive pulmonary disease, particularly when
cholinergic tone is evident
Bronchial asthma- potent inhibitors of secretions
Reduce hyper motility states of the urinary bladder and
GIT
Parkinsonism diseases- with levodopa

Motion sickness
Bradycardia
Atropine, scopolamine, cyclopentolate and tropicamide are
tertiary amines that reach the iris and ciliary body after
topical application to the eye.
Shorter-acting antimuscarinics (cyclopentolate and
tropicamide) have largely replaced atropine due to
prolonged mydriasis observed with atropine (14 days versus
24 hours with other agents).

Atropine
It is tertiary amine
Well absorbed from the GIT, conjunctiva and can cross the
BBB
It used as pre anesthetic medication –
o to reduce the amount of secretion
o to prevent excessive vagal tone due to anesthesia.
As antispasmodic in cases of intestinal, biliary, and renal
colic
Heart block, eye ,hyperhidrosis (too much sweating)
Antidote for cholinergic agonists

Side effects
 Dryness of the mouth, sandy eyes, tachycardia and blurred
vision, retention of urine
 Photophobia
 Hyperthermia-dangerous in children.
 Almost no detectable effect on the CNS in doses that are
used clinically
 Low doses of cholinesterase inhibitors such as
physostigmine may be used to overcome atropine toxicity
 Contraindications: Glaucoma, prostatic hyperplasia and
bladder outlet obstruction

Hyoscine (scopolamine)
• It is tertiary amine and has the same effect as atropine
except for some differences :-
• Unlike with atropine, CNS effects are observed at therapeutic
doses and has longer duration of CNS action
• It has certain advantages over atropine.
• better for preanesthetic medication because of strong
antisecretory and antiemetic action and also brings about
amnesia
• It can be used for short- travel motion sickness
• It is similar to atropine in pk and adverse effects

Ipratropium
• A quaternary amine derivative of atropine
• Given via inhalation route
• Clinical indications
• Asthma in patients who are unable to take adrenergic
agonists
• Chronic obstructive pulmonary disease
• Tropicamide and cyclopentolate
• Like atropine to bring about mydriasis and cyclopegia
but preferred b/c of very short duration of effect
than atropine

Summary of anti muscarinic

Anti-nicotinics
A. Ganglionic blockers
 They act on the nicotinic receptors of both sympathetic and
parasympathetic autonomic ganglia
 They have no selectivity
 The responses observed are complex and unpredictable,
making it impossible to achieve selective actions.
 Therefore, ganglionic blockade is rarely used therapeutically.
 There are often serve as tools in experimental pharmacology

Nicotine
 Depending on the dose, nicotine depolarizes autonomic
ganglia, resulting first in stimulation and then in paralysis
of all ganglia.
 It is effective in reducing the craving for nicotine in
people who wish to stop smoking
 It is available as patches, lozenges, gums, and other forms
Trimethaphan and mecamylamine
 They primarily used to lower blood pressure in emergency
situations
 They can be absorbed when given orally

B. Neuromuscular blocking drugs
• Affect synaptic transmission only at skeletal muscle
• Block synaptic transmission at the neuromuscular junction,
but does not affect nerve transmission, action potential
generation
• Neuromuscular blockers are clinically useful during surgery
to facilitate tracheal intubation
to provide complete muscle relaxation at lower
anesthetic doses
allowing for more rapid recovery from anesthesia
reducing postoperative respiratory depression

NMB are classified as:
• Depolarizing muscle relaxants eg Succinylcholine
• Non-depolarizing muscle relaxants eg: tubocurarine
Pharmacokinetics
 All neuromuscular blockers are quaternary compounds.
 They are not absorbed in GIT, do not cross placental, and BBB.
 They are injected intravenously
 Many of the drugs are not metabolized; their actions are
terminated by redistribution
 The unchanged drug is excreted in urine, and bile.

Non –depolarizing NMB
 At low doses, they interact with the nicotinic receptors to
prevent competitively the binding of Ach
 But with no significant effect on ion channels of the end plate
 At this time their action can be reversed by increasing the
concentration of ACh in the synaptic gap. eg by neostigmine
 This strategy often used to shorten the duration of the
neuromuscular blockade in anaesthesia

 At high doses, they block cholinoreceptors at motor end
plate
 They block the ion channels of the end plate further
weakening muscles
 This reduces the ability of AChEIs to reverse the actions
of non depolarizing muscle relaxants
 The first muscles to be affected are eye muscles, muscles
of the face, limbs and pharynx (causing difficulty in
swallowing).
 Respiratory muscles are the last to be affected and the
first to recover.

Depolarizing NMB agents
 Attaches to the nicotinic receptor and acts like
acetylcholine to depolarize the junction but eventually
blocking it
 Unlike acetylcholine which is instantly destroyed by
AChE, the depolarizing agent persists at high
concentrations in the synaptic cleft remaining attached
to the receptor for a relatively longer time and providing
a constant stimulation of the receptor
 The depolarizing agent first causes the opening of the
sodium channel associated with the nicotinic receptors,
which results in depolarization of the receptor , initially
produces short-lasting muscle fasciculations (Phase I) ,
continued binding gives way to gradual repolarization as
the sodium channel closes or is blocked.
 This causes a resistance to depolarization (Phase II) and
followed within a few minutes by paralysis.

Mechanism of action of depolarizing neuromuscular-blocking
drugs

 Succinylcholine
• Its brief duration of action (several minutes) results
from redistribution and rapid hydrolysis by plasma
cholinesterase
Indications
 Useful when rapid tracheal intubation is required during
induction of anesthesia
 Does not require reversal rather cholinesterase inhibitors
(neostigmine) can prolong the depolarizing block (because these
agents also inhibits the (pseudocholinesterase)

Adverse effects
 Hyperthermia
In genetically susceptible people
Treated by administration of dantrolene
Given IV when treating an attack of malignant
hyperthermia
Dose-dependent muscle weakness and hepatotoxicity
 Apnea
• In a patient who is genetically deficient in plasma
cholinesterase or has an atypical form of the enzyme due
to paralysis of the diaphragm.

DRUGS ACTING ON THE
SYMPATHETIC NERVOUS
SYSTEM

Drugs acting on the sympathetic
nervous system
Based on the effect on the NS:
a. Sympathomimetics or adrenergic drugs:
- are drugs that mimic the effects of sympathetic
nerve stimulation.
b. Sympatholytics:
- are drugs that inhibit the activity of sympathetic
nerve or that of sympathomimetics.

Sympathomimetic
Catecholamine's
 Have the catechol nucleus
 Have a direct action on
sympathetic effectors cells
through interactions with receptor
 High potency, rapid inactivation,
poor penetration into the CNS
 E.g.adrenaline, noradrenaline,
dopamine
Non catecholamines
Lack the catechol nucleus
May act directly or
indirectly
 Have longer half-lives,
and greater lipid solubility
permits greater access to
the CNS
 Eg. Ephedrine,
phenylephrine

Sympathomimetics
• They can be grouped by mode of action
Direct acting: directly interact with and activate
adrenoreceptors, e.g., adrenaline and
noradrenaline
Indirect acting : their actions are dependent on
the release of endogenous catecholamines.
i. Induction of release, e.g., amphetamine,
tyramine
ii. Inhibition of reuptake,e.g. cocaine, tricyclic
antidepressants
Mixed acting (direct + indirect)..ephedrine

• Sites of action of direct,
indirect, and mixed-acting
adrenergic agonists

Life cycle of noradrenaline

Adrenergic receptors

α1 stimulation
• Contraction of the skin and viscera blood vessels ,nasal
blood vessels ,radial muscle ,smooth muscle of the
sphincters of GIT and urinary bladder
α2 stimulation
• ejaculation, glycogenolysis and gluconeogenesis, lipolysis,
decreased norepinephrine release ,decreased insulin
release and increased platelets aggregation

β 1 stimulation
• In the heart causes
In S.A node : increase HR (+ve chronotropic)
In myocardium tissue : increase contractility
(+ve inotropic)
In conducting system : increase conduction
velocity (+ve dromotropic)
• In kidney cause increased renin release.
• In fat cells (with α1, α2 and β 3) causes increased
lipolysis

β2 stimulation
In the bronchial smooth muscle (bronchodilatation)
In the smooth muscle of blood vessels supplying the
skeletal muscle –vasodilatation.
In the smooth muscle of GIT wall -decreased peristalsis
In the smooth muscle of urinary bladder - relaxation
In the smooth muscle of the uterus - relaxation
In the liver causes increased glycogenolysis and
gluconeogenesis

In the pancreas causes slight increase in glucagon secretion
In ciliary muscle causes relaxation of the ciliary muscle
leading to accommodation for far vision
decrease outflow of aqueous humor
In the ciliary epithelium causes increased production of aqueous
humor
β2 stimulation increase potassium influx

Major effects mediated by α- and β-
adrenoceptors

Sympathomimetic agonists classification

Non selective sympathomimetic agonists
Norepinephrine (NE)
 is a neurotransmitter released from the postganglionic
sympathetic fiber in most organs
 It released from the adrenal medulla (20% of medulla
secretion)
 It is a direct non–selective adrenergic agonist which acts
on all adrenoceptors, except β2
 80% by MAO in presynaptic nerve terminals after
reuptake
 15% by COMT in postsynaptic membrane
 5% reach the blood and metabolized in the liver

Epinephrine (EP)
EP is released from adrenal medulla =80% and in certain
areas of the brain
EP is a direct acting non-selective adrenergic agonist in all
receptors including β2 receptor.
T1/2 = 2 – 5 min
It is given parenterally (SC, I.V and I.M) not orally
Epinephrine is commonly used in clinical practice as
compared to NE.
In bronchial asthma ,cardiogenic shock and anaphylactic
shock

During surgery, is added to the local anesthetic to cause
VC in the surgery area in order to
 Decrease bleeding
 Decrease the amount of local anesthetic which
reach the systemic circulation.
 Therefore, it decrease the cardio depressant
effect of the local anesthetic

Adverse effects
 Hypertensive crisis
 Arrhythmias
 Angina
 Necrosis of the extremities
 Hyperglycemia
 Anxiety, restlessness, headache
, tremor
Contraindications
o Coronary diseases
o Hyperthyroidism
o Hypertension
o Digitalis therapy
o Injection around end
arteries

Dopamine
It is immediate metabolic precursor of NE and
occurs naturally in the CNS as well as in the adrenal
medulla
Its effect on the ß1 have both positive inotropic and
chronotropic effects(medium dose)
At very high doses dopamine activates 1 receptors
on the vasculature, resulting in vasoconstriction
Its dopaminergic receptors activity dilates renal
and splanchnic arterioles by activating dopaminergic
receptors, thus increasing blood flow to the kidneys
and other viscera(low dose)

• T1/2 = 3 – 5 min
• Metabolized by either
• Converted to NE in adrenergic neurons or
• By MAOB in the Liver
• Dopamine is clinically useful in the treatment of shock, in
which significant increases in sympathetic activity might
compromise renal function

Dobutamine
 It is direct acting β1 – selective agonist (only)
 Given only parenterally (not orally)
 It is metabolized in the liver by oxidative deamination
 T1/2 = 10 – 15 min
 It exerts a greater effect on the contractile force of the
heart relative to its effect on the heart rate than does
dopamine, so it has less arrhythmogenic effects than
dopamine
 Inotropic agent for heart failure; in septic and cardiogenic
shock.

β2 – selective agonist
Albuterol and terbutaline are short-acting ß2 agonists
used primarily as bronchodilators .
They produce equivalent bronchodilation with less cardiac
stimulation when compared to non-selective bronchodilators
They have longer duration of action than isoproterenol
because they are not metabolized by COMT
They are effectively administered either orally or SC

 Salmeterol and formoterol are ß2-adrenergic selective, long-
acting bronchodilators
 The agents of choice for treating nocturnal asthma in
symptomatic patients taking other asthma medications
 Single inhalation dose has bronchodilation over 12 hours,
compared with less than 3 hours for albuterol
 Salmeterol has a somewhat delayed onset of action than
formoterol

Selective α1–agonist
Phenylephrine
It is relatively selective directly acting α1–agonist
It has longer duration of action than other catecholamines
It is not-catecholamine and thus not metabolized by COMT
As a mydriatic agent to examine the fundus of the eye
As a decongestant ,used as nasal drops to relief congestion
As a vasopressor agent in case of hypotension

Mixed-acting adrenergic agent
Ephedrine
• Release stored NE and interact with  and ß
adrenoceptors
• It is often used prophylactically to prevent asthmatic
attacks , as a nasal decongestant, and as a mydriatic
• Nocturnal enuresis (bedwetting)
• Narcolepsy (uncontrollable tendency to fall asleep at
any time)

Adrenergic Antagonists
• Prevent stimulation of
adrenergic receptors from
neurotransmitters or drugs

Non selective α antagonists
Phenoxybenzamine: /pentolamine
 Nonselective, linking covalently to both 1-postsynaptic and 2-
presynaptic receptors
 It blocks irreversible and noncompetitive
 The drug has been unsuccessful in maintaining lowered blood
pressure in hypertension and has been discontinued for this
purpose.
 Treatment of pheochromocytoma - tumor consisting of cells that
release varying amounts of norepinephrine and epinephrine into
the circulation
 May induce reflex tachycardia and is contraindicated in patients
with decreased coronary perfusion.

a1 antagonist
Prazosin, dexazosin ,terazosin
 They are selective competitive blockers of the 1
receptor
 They are useful in the treatment of hypertension
 The first dose of these drugs produces an exaggerated
orthostatic hypotensive response that can result in
syncope (fainting)
 It may be minimized by adjusting the first dose to one-
third or one-fourth of the normal dose and by giving the
drug at bedtime
• BPH-reduce urinary hesitancy and prevent urinary
retention in men

Therapeutic applications of alpha blockade
 Treatment of hypertension
 Reversal of toxicity caused by alpha1 agonists
 Treatment of pheochromocytoma ( rare adrenaline-
producing tumor that arises from the adrenal glands.)
 BPH- enlargement of prostate gland
 Raynaud’s disease- restriction of blood supply to fingers
making it white, cold and numb

Adverse effect of alpha blockade
Orthostatic (postural) hypotension
Nasal congestion
Inhibition of ejaculation
Reflex tachycardia

Beta blockers
β1-selective:
Metoprololol
Acebutolol
Atenolol
Betaxolol
Esmolol
β-non selective blockers:
Propranolol
Pindolol
Timolol
Nadolol

• Partial agonist activity (“intrinsic sympathomimetic activity”)
• It may be an advantage in treating patients with asthma
• because these drugs (eg, pindolol, acebutolol)—at least
in theory—are less likely to cause bronchospasm.
• In contrast, full antagonists such as propranolol are more
likely to cause severe bronchospasm in patients with
airway disease.

Local anaesthetic activity
 Local anaesthetic activity (“membrane-stabilizing
activity”) is a disadvantage when β blockers are used
topically in the eye
because it decreases protective reflexes and
increases the risk of corneal ulceration.
 Local anaesthetic effects are absent from timolol and
several other β blockers that are useful in glaucoma.

• It is useful in hypertensive patients with impaired pulmonary
function -beta1 antagonist
• It is also useful in diabetic hypertensive patients who are
receiving insulin or oral hypoglycemic agents- beta1 antagonist
• Hypertension ,angina pectoris, cardiac arrhythmias and
glaucoma(Therapeutic application)
Bradycardia ,reduction of cardiac output and congestive heart
failure(beta1)
Bronchial constriction and inhibition of glycogenolysis (beta2)
C/Is: HF, DM, asthma

α2 – selective agonist
 Methydopa ,guanandrel guanfacina and clonidine
They are sympatholytic agent used in treatment of
hypertension
They acts centrally at presynaptic α2-adrenoceptor.
This leads to decrease in NE release and to decrease in
TVR.

Adrenergic neuronal blockers
Reserpine
• It blocks the Mg2+/adenosine triphosphate dependent
transport of norepinephrine
• It causes the ultimate depletion of NE
• Sympathetic function, in general, is impaired because of
decreased release of norepinephrine
• It has a slow onset, a long duration of action, and
effects that persist for many days after
discontinuation

Autonomic nervous system pharmacology

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Autonomic nervous system pharmacology

Similar to Autonomic nervous system pharmacology (20)

Recently uploaded

Recently uploaded (20)

Autonomic nervous system pharmacology

Editor's Notes