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Propranolol — Pharmacological Account

Source: Slides by Mrs. Sugandha Chaudhari | Katzung's Basic and Clinical Pharmacology, 16th Edition | The Harriet Lane Handbook, 23rd Edition

1. Drug Classification & Receptor

Propranolol is a non-selective β-adrenoceptor blocker — it blocks both β₁ and β₂ adrenergic receptors with equal affinity. It has no intrinsic sympathomimetic activity (ISA) and possesses membrane-stabilising (local anaesthetic) properties at high doses.

β₁ receptors → heart (SA node, AV node, myocardium)
β₂ receptors → bronchi, peripheral blood vessels, liver, skeletal muscle

2. Pharmacological Actions

A. Cardiovascular System (CVS)

Negative inotropic and chronotropic effects — reduces heart rate and force of contraction → decreases cardiac output (CO)
Slows SA node automaticity and AV node conduction
Reduces myocardial oxygen consumption → beneficial in angina
Decreases blood pressure primarily by reducing cardiac output
Also inhibits renin secretion (β₁-mediated) → suppresses renin-angiotensin-aldosterone system → antihypertensive effect

B. Peripheral Vasculature

Blockade of β₂ receptors prevents peripheral vasodilation → initial rise in peripheral resistance
Fall in BP from reduced CO eventually compensates
Can cause cold extremities due to unopposed α-receptor vasoconstriction

C. Respiratory

Blockade of β₂ receptors → bronchoconstriction
Not considerable in healthy individuals but dangerous in asthma
Contraindicated in asthma; COPD patients tolerate it better
β₁-selective drugs are preferred when a beta-blocker is needed in airway disease

D. Eye

Reduces intraocular pressure (IOP) by decreasing aqueous humour production → used in glaucoma

E. CNS

No major CNS effects except behavioural changes, forgetfulness, nightmares
Suppresses anxiety (used in situational anxiety/performance anxiety)

F. Skeletal Muscle

Reduces tremor (inhibits β₂-mediated vasodilation and lipolysis/glycogenolysis in muscle)
Reduces exercise capacity

G. Metabolic — Lipid

Inhibits sympathetic stimulation of lipolysis → ↑ free fatty acids and ↑ triglycerides
↑ LDL/HDL ratio (adverse metabolic profile)

H. Metabolic — Carbohydrate

Inhibits glycogenolysis (β₂-mediated) in heart, muscle, and liver
Inhibits glucagon secretion
Delays recovery from insulin-induced hypoglycaemia
Warning signs of hypoglycaemia (tachycardia, tremor) are masked
Patients with insulin-dependent diabetes must be monitored — pronounced hypoglycaemia may occur
β₁-selective agents are much safer in diabetics

I. Blocks Action of Isoproterenol

Isoproterenol's CVS effects are antagonised by propranolol without causing CVS stimulation

J. Sodium Retention

Reduced BP → ↓ renal perfusion → ↑ renal sodium retention → compensatory ↑ BP
This is why beta-blockers are combined with diuretics in hypertension

3. Pharmacokinetics

(Source: Slides; Katzung 16th ed.)

Parameter	Detail
Absorption	Well absorbed orally; peak concentration 1–3 hours
First-pass metabolism	Extensive hepatic first-pass — oral:parenteral ratio 40:1
Bioavailability	High inter-individual variation; higher with food
Metabolism	Hepatic blood flow–dependent; propranolol itself decreases hepatic blood flow → higher bioavailability on chronic use
Dose	10–80 mg tablets; 40–160 mg/day
Formulations	Standard and sustained-release preparations available

4. Uses / Clinical Indications

Indication	Mechanism
Hypertension	↓ CO + ↓ renin secretion
Angina pectoris	↓ heart rate and contractility → ↓ O₂ demand
Cardiac arrhythmias	Slows SA/AV node; class II antiarrhythmic
Post-MI (secondary prevention)	Reduces mortality
Heart failure (select cases)	Reduces mortality with careful titration
Migraine prophylaxis	Reduces frequency of attacks
Thyrotoxicosis	Controls sympathomimetic symptoms (tachycardia, tremor)
Essential tremor	β₂ blockade in skeletal muscle
Phaeochromocytoma	Only after α-blockade (never alone)
Glaucoma	Reduces aqueous humour production
Anxiety / situational	Blunts peripheral sympathetic symptoms
Infantile haemangioma	Promotes involution (2–3 mg/kg/day) (Harriet Lane, 23rd ed.)

5. Adverse Drug Reactions (ADRs) & Contraindications

(Source: Slides — Propranolol ADRs and CI)

ADR	Mechanism
Bradycardia / Heart block	β₁ blockade at SA/AV node
Precipitation of CCF/Oedema	Loss of sympathetic support; negative inotropy
Bronchoconstriction / Bronchospasm	β₂ blockade; life-threatening in asthma/COAD
Cold hands and feet	Peripheral vasoconstriction, worsening PVD
Tiredness, reduced exercise capacity	β₂ blockade in skeletal muscle
Hypoglycaemia (masked)	Inhibits glycogenolysis; masks warning signs
↑ Triglycerides, ↑ LDL, ↓ HDL	Metabolic risk for coronary artery disease
Variant angina exacerbation	Unopposed coronary α-receptor constriction
Withdrawal syndrome	β-receptor up-regulation → rebound tachycardia, hypertension, angina exacerbation — never stop abruptly (Katzung 16th ed.)
GIT upset, nightmares, forgetfulness, sexual distress	CNS and peripheral effects

Absolute contraindications: Asthma, severe bradycardia, AV block (2nd/3rd degree), cardiogenic shock, uncontrolled heart failure.

6. Drug Interactions

(Source: Slides — Drug Interactions)

Combination	Effect
Propranolol + Insulin	Delayed recovery from hypoglycaemia; warning signs suppressed
Propranolol + Alpha agonists	Rise in BP (loss of β₂-mediated vasodilation + α vasoconstriction)
NSAIDs + Propranolol	Attenuation of antihypertensive effect

Summary

Propranolol is the prototype non-selective β-blocker, blocking both β₁ and β₂ receptors. Its cardiovascular benefits (angina, hypertension, arrhythmia, post-MI) are well established, but its non-selectivity makes it unsuitable in asthma, diabetes, and peripheral vascular disease where β₁-selective agents (metoprolol, atenolol) are preferred.

References:

Slides: Mrs. Sugandha Chaudhari (Propranolol — Blocks beta-1 and beta-2 receptor, slides 1–24/33)

Katzung's Basic and Clinical Pharmacology, 16th Edition, pp. 287–289

The Harriet Lane Handbook, 23rd Edition (Johns Hopkins), pp. 1316–1317

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