This PPT includes Anti Adrenergic drugs also known as Sympatholytics. This includes Alpha Blockers and Beta Blockers

1. ANTI-ADRENERGIC DRUGS
SYMPATHOLYTICS
PREPARED BY: JEGAN.S.NADAR

2. • These are drugs which antagonize the receptor action of
adrenaline and related drugs
• They are competitive antagonists at α or β or both α and β
adrenergic receptors
Jegan

3. α-ADRENERGIC BLOCKING DRUGS
Jegan

4. α-ADRENERGIC BLOCKING DRUGS
• These drugs inhibit adrenergic responses mediated through the α
adrenergic receptors without affecting those mediated through
β receptors
Jegan

5. Jegan

6. GENERAL EEFECTS OF α-BLOCKERS
1.BLOOD PRESSURE
• Blockade of α1-receptor
• Vasodilation
• Decrease in peripheral resistance
• Peripheral pooling of blood
• Venous return and Cardiac output decreases
• BP falls
• Hypotension occurs on standing
Jegan

7. 2.REFLUX TACHYCARDIA
Reflux tachycardia occurs due to
• Fall in mean arterial BP
• Release of NA due to blockade of pre-synaptic α2 receptor
3.NASAL STIFFNESS AND MIOSIS
• Blockade of α-receptor in nasal blood vessels and in radial muscles
of iris
Jegan

8. 4.RENIN RELEASE
• Reduced BP
• Hypotension
• Renal blood flow decreases
• GFR decreases
• Complete reabsorption of sodium and water
• Retention of sodium and increase in blood volume
• Renin release
Jegan

9. 5. SMOOTH MUSCLE
• Intestinal motility is increased
• loose motion may occur.
• Tone of smooth muscle in bladder trigone, sphincter and prostate is
reduced by blockade of α1 receptors
6. EJACULATION
• Contraction of vas deferens coordinates ejaculation through α-
receptor
• Αlfa-blockers can inhibit ejaculations
• Impotence
Jegan

10. PHENOXYBENZAMINE
• It cyclizes spontaneously in the body giving rise to a highly reactive
ethyleniminium intermediate which reacts with α-adrenoceptors
• The α blockade is of nonequilibrium (irreversible) type
• Effects lasts for 3–4 days till fresh receptors are synthesized.
• The fall in BP caused by phenoxybenzamine is because venodilatation is more
prominent than arteriolar dilation
Jegan

11. PHENOXYBENZAMINE
• Phenoxybenzamine is lipid soluble, penetrates brain and can produce CNS
stimulation, nausea and vomiting on rapid i.v
• However, oral doses produce depression, tiredness and lethargy
• Major side effects are postural hypotension, palpitation, nasal blockage, miosis,
inhibition of ejaculation
Jegan

12. PHENTOLAMINE
• This is a rapidly acting α blocker with short duration of action (in minutes).
• It equally blocks α1 and α2 receptors—NA release is increased
• Venodilatation predominates over arteriolar dilatation.
• It is used as a quick and short acting α blocker for diagnosis and intraoperative
management of pheochromocytoma and for control of hypertension due to
clonidine withdrawal, cheese reaction, etc
Jegan

13. PRAZOSIN
• It is first of the highly selective α1 blockers having α1 : α2 selectivity ratio 1000:1.
• All subtypes of α1 receptor (α1A, α1B, α1D) are blocked equally.
• It blocks sympathetically mediated vasoconstriction and produces fall in BP
• NA release is not increased due to absence of α-2 blockade.
• Used in management of Hypertension
Jegan

14. β-ADRENERGIC BLOCKING DRUGS
Jegan

15. PROPRANOLOL IS THE PROTOTYPE

16. PHARMACOLOGICAL ACTION OF PROPRANOLOL
1. Cardiovascular System
A) Heart
• It decreases HR
• Force of contraction decreases
• CO decreases
• Cardiac work and oxygen consumption are reduced as the product of heart
rate and aortic pressure decreases.
Jegan

17. • Total coronary flow is reduced (blockade of dilator β receptors), but this is
largely restricted to the subepicardial region, while perfusion of the
subendocardial area (which is the site of ischaemia in angina patients) is not
affected.
• The overall effect in angina patients is improvement of O2 supply/demand
status; Exercise tolerance is increased.
• Negative inotropic and chronotropic action.
• Prolong AV conduction (delay)
• Diminish phase 4 depolarization  suppressing automaticity(of ectopic focus)
Jegan

18. B) BLOOD VESSELS
• Propranolol has no direct effect on blood vessels and there is little acute
change in BP
• Decrease in cardiac output decreases T.P.R gradually
• Fall in both systolic and diastolic B.P
• Other mechanisms that may contribute are:
 Reduced NA release from sympathetic terminals due to blockade of β
receptor
 Decreased renin release from kidney (β1 mediated)
Jegan

19. 2. RESPIRATORY TRACT
• Blocks β-2 receptor
• Bronchocontriction
• Precipitation of asthmatic attack in asthma patient
• No significant effect in normal individual
3. CNS
• No central effects are produced by propranolol.
• However, subtle behavioural changes, forgetfulness, increased dreaming and
nightmares have been reported with long-term use of relatively high doses
Jegan

20. 4. LOCAL ANAESTHETIC
• Propranolol is a potent local anaesthetic like lidocaine,
• But is not clinically used for this purpose because it causes irritation at the
injected site
5. METABOLIC
• Propranolol blocks adrenergically induced lipolysis
• It also inhibits glycogenolysis in heart, skeletal muscles and in liver
Jegan

21. 6. EYE
• Instillation of propranolol and some other β blockers reduces secretion of
aqueous humor, i.o.t. is lowered.
• There is no consistent effect on pupil size or accommodation.
7. UTERUS
• Relaxation of uterus in response to isoprenaline and selective β2 agonists is
blocked by propranolol.
• However, normal uterine activity is not significantly affected.
Jegan

22. PHARMACOKINETIC
• Propranolol is well absorbed after oral
administration,
• But has low bioavailability due to high
first pass metabolism in liver
• Propranolol is lipophilic and penetrates
into brain easily.
DRUG INTERACTION
• Additive depression of sinus node and A-V
conduction with digitalis and verapamil —
cardiac arrest can occur
• Indomethacin and other NSAIDs attenuate
the antihypertensive action of blockers
• Cimetidine inhibits propranolol metabolism

23. ADVERSE EFFECT
• Bradycardia
• Propranolol worsens chronic obstructive lung disease, can precipitate life-
threatening attack of bronchial asthma: contraindicated in asthmatics
• Plasma lipid profile is altered on long term use
• Withdrawal of propranolol after chronic use should be gradual, otherwise
rebound hypertension, worsening of angina and even sudden death can occur
• Tiredness and reduced exercise capacity
• Propranolol is contraindicated in partial and complete heart block: arrest may
occur

24. Thank You