This document discusses adrenergic antagonists, which are drugs that inhibit the function of adrenergic receptors. There are five types of adrenergic receptors divided into alpha and beta receptors. Adrenergic antagonists are classified as alpha-selective, beta-selective, competitive, or non-competitive. Common adrenergic antagonists are discussed along with their mechanisms of action, pharmacological effects, clinical uses, pharmacokinetics, and adverse effects. Key uses include treating hypertension, congestive heart failure, pheochromocytoma, and benign prostatic hyperplasia.

1. Adrenergic Antagonist
Laith J. Al-Asadi

2. Adrenergic Antagonist
• An adrenergic antagonist is a drug that
inhibits the function of adrenergic
receptors.
• There are five adrenergic receptors, which
are divided into two groups :

3. Adrenergic Receptors
• The first group of receptors are the alpha
(α) adrenergic receptors.
There are α1 and α2 receptors.
• The second group contains the beta (β)
adrenoceptors.
There are only β1, β2, and β3 receptors

4. Classification of
Adrenoceptors Blockers
1- alpha vs. beta
• Adrenoceptors are classified as α, β, or
dopamine receptors
• These groups are further subdivided into
subgroups.

6. Classification of
Adrenoceptors Blockers
2- competitive vs. non competitive
2-A: Competitive
• While only a few α-adrenergic
antagonists are competitive, all β-
adrenergic antagonists are competitive
(reversible) antagonists

7. Classification of
Adrenoceptors Blockers
• Adrenergic competitive antagonists are
shorter lasting than the other types of
antagonists
2-B: non-competitive antagonists
• can either bind to the ligand site or other
site called the allosteric site

8. Classification of Adrenoceptors
Blockers
• The binding of a non-competitive
antagonist is irreversible.
• If the non-competitive antagonist binds to
the allosteric site and an agonist binds to
the ligand site, the receptor will remain
inactive ex: phenoxybenzamine

9. Classification of
Adrenoceptors Blockers
3- selective vs. non selective
Alpha1-selective Prazosin
Alpha2-selective Yohimbine
Beta1 – selective metoprolol

11. Mechanism of Action
• Phenoxybenzamine binds covalently to the
α receptor, thereby producing an
irreversible blockade.
• The other agents are competitive
antagonists, and their effects can be
surmounted by increased concentrations
of agonist

12. Pharmacological effects
 cardiovascular system:
• a reduction in vascular tone with a
reduction of both arterial and venous
pressures.

13. Pharmacological effects
 Epinephrine reversal
• is a predictable effect in a patient who has
received an α blocker. The term refers to a
reversal of the blood pressure effect of
large doses of epinephrine

14. Pharmacological effects
Urinary system
• α1 blockers (selective), tamsulosin,
prazocin and silodosin are also used to
reduce urinary hesitancy and prevent
urinary retention in men with benign
prostatic hyperplasia.

15. Clinical uses
pheochromocytoma
Overdose with drugs of abuse such as
amphetamine, cocaine.
Hypertension.
Congestive heart failure.
urinary retention in men with benign prostatic
hyperplasia.

16. Pharmacokinetics
• Phentolamine has a duration of action of
2–4 h when used orally and 20–40 min
when given parenterally. Prazosin and the
other α1
• selective blockers act for 8–24 h.

17. Pharmacokinetics
• Phenoxybenzamine has a short
elimination half-life but a long duration of
action about 48 hr. because it binds
covalently to its receptor.

18. Adverse effects
The most important adverse effects are :
• orthostatic hypotension.
• marked reflex tachycardia. (non selective)
• In patients with coronary disease, angina may
be precipitated by the tachycardia.
• Inhibition of ejaculation.
• Oral administration of some of these drugs can
cause nausea and vomiting.

19. α1 blockers
Phentolamine
phenoxybenzamine
Tamsulosin
Prazocin
Alfazocin
Doxazocin
Tolazolin
Terazocin

20. Beta adrenergic blockers
• All of the β blockers used clinically are
competitive pharmacologic antagonists.
• β blockers usually classified into subgroups
on the basis of
 β1 selectivity
 partial agonist activity
 local anesthetic action
 lipid-solubility

21. Receptor selectivity—Beta1
• (β1 block > β2 ) acebutolol, atenolol, esmolol,
metoprolol.
• This property may be an advantage when
treating patients with asthma.
• Nadolol, propranolol, and timolol are typical
nonselective β blockers.
• Labetalol and carvedilol have combined α- and
β-blocking actions.

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

23. Local anesthetic 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 anesthetic effects are absent from timolol
and several other β blockers that are useful in
glaucoma.
• Acebutolol and betaxolol

24. Pharmacokinetics
• Most of the systemic agents have been
developed for chronic oral use, but
bioavailability and duration of action vary
widely .

25. Pharmacokinetics
• Esmolol is a short-acting ester β blocker that is
used only parenterally.
• Nadolol is the longest-acting β blocker.
• Acebutolol, atenolol, and nadolol are less
lipid-soluble than other β blockers and probably
enter the central nervous system (CNS) to a
lesser extent

26. Clinical uses
• The treatment of open-angle glaucoma
involves the use of several groups of
autonomic drugs as well as other agents
• The cardiovascular applications of β
adrenergic blockers—especially in
hypertension, angina, and arrhythmias
are extremely important

27. Clinical uses
• Some, but not all, β blockers can reduce
morbidity and mortality when used
properly in heart failure like labetalol,
carvedilol, and metoprolol
• Pheochromocytoma is sometimes
treated with combined α- and β-blocking
agents (eg, labetalol), especially if the
tumor is producing large amounts of
epinephrine as well as norepinephrine.

28. Adverse effects
• Bradycardia.
• Atrioventricular blockade.
• Heart failure.
• Asthma attacks.
• Masking symptoms of hypoglycemia.
• Cold extremities.
• CNS adverse effects include sedation.
fatigue, and sleep alterations.

29. β blockers
Propranolol Nebivilol
Atenolol Oxprenolol
Metoprolol Timolol
Pindolol Nadolol
Esmolol Acebutolol
Sotalol Talinolol
Betaxolol Labetalol Carvedilol

30. Thank you