Hello friends. In this PPT I am talking about autonomic nervous system. If you like it, please do let me know in the comments section. A single word of appreciation from you will encourage me to make more of such videos. Thanks. Enjoy and welcome to the beautiful world of pharmacology where pharmacology comes to life. This video is intended for MBBS, BDS, paramedical and any person who wishes to have a basic understanding of the subject in the simplest way.

1. Adrenergic drugs
Dr. Karun Kumar
Assistant Professor
Dept. of Pharmacology

2. Noradrenergic transmission
• Restricted to the sympathetic division of the ANS
1. Norepinephrine  Postganglionic sympathetic
neurons sites (except at sweat glands, hair
follicles and some vasodilator fibres) and in
certain areas of brain.
2. Epinephrine  Adrenal medulla
3. Dopamine  Renal and mesenteric vasculature

3. Synthesis of
catecholamines

4. Location of adrenergic receptors
1. α1 Smooth muscle, exocrine glands, CNS
2. α2  Presynaptic neurons, various tissues and
blood platelets
3. β1  Heart, JG cells in kidney
4. β2  Bronchi, blood vessels, uterus, liver, GIT,
urinary tract, eye
5. β3 Adipose tissue

10. Adrenergic responses mediated
through α and β receptors

12. After qisses (kisses), you get a qiq (kick)
out of siq (sick) sqs (super qinky sex)

15. Baroreceptor reflex

16. • When a drug or a physiologic action increases
blood pressure, this activates stretch receptors
(mechanoreceptors) located in the aortic arch and
in the carotid sinus at the bifurcation of the carotid
artery
• Receptor activation initiates impulses that travel via
afferent nerves to the brain stem vasomotor center
• Stimulation of the vagal motor nucleus (via nerves
from the solitary tract nucleus) leads to an increase
in vagal (parasympathetic) outflow, a decrease in
heart rate, and a decrease in the sympathetic nerve
outflow from the vasomotor center
• The effect on the heart rate is called reflex
bradycardia

17. Effect of A, NA & Iso on BP & HR

18. Vasomotor reversal of Dale

19. • Phenoxybenzamine is an irreversible antagonist
whereas Phentolamine and Tolazoline are
reversible blockers of α1 and α2 receptors 
Vasodilation and postural hypotension
• Reflex increase in sympathetic discharge and
increased sympathetic outflow (due to blockade of
α2 receptors) are responsible for marked
tachycardia seen with the use of these agents

20. • Use of these drugs before adrenaline results in
vasomotor reversal of Dale
• Intravenous injection of adrenaline normally causes
increase in blood pressure (α effect) followed by
prolonged fall (β2 effect)
• If it is administered after giving α blockers, only fall
in BP is seen (vasomotor reversal of Dale)

21. Classification

22. Administration
• CAs are absorbed from the intestine but are rapidly
degraded by MAO & COMT present in the intestinal
wall and liver (orally inactive)
• Adrenaline (epinephrine) is administered by s.c. or
i.m. injection in a dose of 0.2–0.5 mg; action lasts
0.5–2 hours.
• In dental practice, it is used as a local vasoconstr.
added to lidocaine in a concentration of 1 in
200,000 to 80,000 for dental anaesthesia.

23. Dopamine
• Low doses (< 2 μg/kg per min)  D1 dopaminergic
receptors in renal, mesenteric, and coronary
vascular beds (vasodilation); activates adenylyl
cyclase in vascular smooth muscle cells, leading to
↑ cAMP levels and vasodilation
• Moderate dose (2–10 μg/kg per min)  β1 recept.
(positive inotrope)
• Higher dose (>10 μg/kg per min)  α1 receptors
(vasoconstriction)

24. Adrenaline
Uses (ABCDE)
1. Anaphylactic shock (DOC)  0.5 mg (0.5 ml of 1
in 1000 solution for adult) i.m.
2. Bronchial asthma
3. Cardiac arrest  10 ml of 1:10000 i.v.
4. Control of local bleeding  Adr 1 in 10,000
5. During LA combined with Lignocaine (1:50,000 or
1:2,00,000)
6. To control Epistaxis

25. Adrenaline in Anaphylactic shock

26. • The LA often fails to afford adequate pain control in
inflamed tissues (like infected tooth)
• The likely reasons are:
1. Inflammation lowers pH of the tissue— greater
fraction of the LA is in the ionized form hindering
diffusion into the axolemma
2. Blood flow to the inflamed area is increased—the
LA is removed more rapidly from the site
3. Effectiveness of Adr injected with the LA is
reduced at the inflamed site
4. Inflammatory products may oppose LA action

27. • Addition of a vasoconstrictor, e.g. adrenaline
(1:50,000 to 1:200,000):
1. Prolongs duration of action of LAs by decreasing
their rate of removal from the local site into the
circulation
2. Enhances the intensity of nerve block
3. Reduces systemic toxicity of LAs: rate of
absorption is reduced and metabolism keeps the
plasma concentration lower

28. 4. Provides a more bloodless field for surgery
5. Increases the chances of subsequent local tissue
edema and necrosis as well as delays wound healing
by reducing oxygen supply and enhancing oxygen
consumption in the affected area
6. May raise BP and promote arrhythmia in
susceptible individuals

29. Adverse Effects
1. Transient restlessness, headache, palpitation,
anxiety, tremor and pallor may occur after s.c./
i.m. injection of Adr
2. Marked rise in BP leading to cerebral
haemorrhage, ventricular tachycardia/fibrillation,
angina, myocardial infarction are the hazards of
large doses or inadvertant i.v. injection of Adr

30. Contraindications
1. Adr is contraindicated in hypertensive,
hyperthyroid and angina patients
2. Adr should not be given during anaesthesia with
halothane (risk of arrhythmias) and to patients
receiving β blockers (marked rise in BP can occur
due to unopposed α action)
3. Adr mixed local anaesthetic should be used very
cautiously for dental anaesthesia in patients with
heart disease

31. Dobutamine
• Selective β1 rec. agonist
• Prominent action  ↑ force of cardiac contraction
and output, without significant change in heart
rate, peripheral resistance and BP
• Uses
1. Pump failure accompanying myocardial infarction
2. Cardiac surgery
3. Short term management of severe congestive
heart failure

32. Phenylephrine
• Selective α1 agonist (↑ BP by causing
vasoconstriction)
• Uses
1. Nasal decongestant
2. Fundus examination (cycloplegia not required)