1. β – ADRENERGIC BLOCKERS

2. β -Adrenergic blockers
All are competitive antagonists at β receptor.
Classification
ISA MSA
( Partial agonist )
I) Nonselective (β1 β2 )
Alprenolol, oxprenolol
Propranolol
Pindolol
Sotalol, Timolol, Nadolol
Nonselective with additional α – blocking action
Labetalol
Carvedilol
II) Cardioselective (β1)
Acebutolol
Metoprolol, Esmolol
Betaxolol, Atenolol

3. Pharmacological actions
III) β2 – Selective blocker- Butoxamine
( only used for research purpose )
IV) β1 Selective – β blocker with β2 agonistic activity
Celiprolol
Pharmacological actions
Heart –
block β1 receptors
force of contraction
C.O.
H.R
Conduction across A-V node
refractory period
Decrease oxygen requirement
Decrease automaticity

4. Blood vessels
No direct action
P.R. may increase initially dlt. Blockade of β2 mediated vasodilatation
On prolonged administration –P.R. es.
Blood pressure
B.P = C. O X P.R
Decrease in B.P
a) Decrease C.O by blocking β1 receptors present on heart.
b) Decrease in P.R.
c) Decrease release of NE from adrenergic neurons peripherally
d) Decrease central symp- outflow
e) Decrease renin release by blocking β1 receptors present on JG
apparatus.
f) Parse mild vasodilatory action

5. Adverse effects Respiratory tract
Block β2 receptors present on tracheal bronchial tree.
Bronchoconstriction
Metabolic
Inhibit glycogenolysis
TG levels
Eye-
Decrease aqueous humor secretion
Adverse effects
CNS- excessive dreaming
Nightmares
RS- Bronchial asthma
CVS- Myocardial insufficiency –CCF –dlt block of sympathetic support to
the heart.
Bradycardia
Partial, complete heart block
Exacerbates variant angina

6. Metabolic –
Lipid - Increase TG. LDL, Decrease HDL- risk of coronary
artery atherosclerosis
CHO- CI in Diabetes mellitus
Decrease exercise capacity
Worsening of PVD
Rapid withdrawal- Rebound hypertension
Supersesitivity Anginal attacks
of β receptors Arrhythmias
Β1 selective blockers
Bronchial asthma
Diabetes mellitus
Peripheral vascular disease
No effect on Lipid profile
Exercise capacity not affected

7. β blockers with intrinsic symptomimitic action
Less bradycardia
Less cardiac depression – in patients with poor cardiac reserve
Withdrawal –less likely the phenomena of supersensitivity
Plasma lipid profile – Not affected
Contraindications
Bronchial asthma
Diabetes mellitus
Hearts rate < 45 / min
Heart block
Variant angina
Drug INTERACTIONS
Should never be combined with calcium channel blockers like verapamil
Delays recovery from hypoglycemia due to insulin. Oral antidiabetic agents .

8. Atenolol Propranolol 1) Selective β1 blocker Nonselective (β1 + β2 )
2) No membrane stabilizing +
3) Less 1st pass effect significant 1st pass effect
4) Low lipid solubility Lipid solubility +++
5) CNS Penetration - ed +
Less CNS S/E
6) Longer duration of action short duration of action
7) Frequency administration Four times a day
Once a day
8) Renal elimination Hepatic elimination

9. THERAPEUTIC USES OF BETA BLOCKERS
1.Hypertension
Atenolol – mg OD
Propranolol -40 – 160 mg / day
2. Angina Pectoris
- Ve onotropic , chronotropic effect
Decrease in C.O
Decrease in O2 requirement of Heart
O2 demand = O2 supply
3. Cardiac arrhythmias –
decrease automaticity of ectopic pacemakers
decrease conduction through A-V node
decrease refractory period of A-V node
Used in supraventricular arrhythmias
4. Myocardial infarction
Limit infarct size by decreasing O2 demand
Myocardial Salvage

10. To prevent re infarction mortality 5.Congestive cardiac failure
B) Prevent arrhythmias
Prophylaxis
To prevent re infarction
mortality
5.Congestive cardiac failure
Endocrine uses
Hyperthyrodism
Pheochromocytoma
CNS USES
1. Chronic prophylaxis of Migraine
Propranolol
2. Essential tremors
3. Anxiety Palpitations,tremors
4. Glaucoma- Timolol %
Betaxolol , Levobunolol
Decreases aq. humour seccretion
Wide angle glaucoma.
Portal Hypertension