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MDP10208 Adrenergic Drugs: Agonists

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Wahizul Muhammad

on 14 December 2015

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Transcript of MDP10208 Adrenergic Drugs: Agonists

Selective Agonists
a1 : Phenylephrine

a2 : Clonidine

ß2 : Salbutamol
a1 selective Adrenergic Agonists
acting alpha agonist
(selectivity for a1, activate ß only at high doses)
main effect is vasoconstriction (which may lead to increased BP)

hypertensive, headache

Nasal decongestant, Mydriatic: as eyedrop to contract dilator muscle of pupil
adrenaline - all alpha & beta receptors
noradrenaline - alpha, ß1 but not ß2
dopamine - lower dose: activate dopamine and ß1 receptors at heart (higher dose: a1 receptors)
Synthetic: dobutamine - mainly ß1
isoprenaline - ß only
MDP10208 Adrenergic Drugs: Agonists
Muhammad Wahizul Haswan B Abdul Aziz
Adrenergic Agonists - Definitions
Sympathomimetic drug/agent - drugs producing similar to effects as activation of the sympathetic nervous system

Catecholamines - drugs (such as nor/adrenaline, dopamine and isoprenaline) which are sympathomimetic amines with a catechol ring (3,4-dihydroxybenzene ring)
Autonomic Pharmacology:
Important organs & receptors
Heart: ß1 increase HR, inotropy
Lung: ß2 dilate bronchioles
Blood vessel: a1 (mainly) vasoconstriction
ß2 dilation at periphery
Uterus: ß2 for relaxation
Adrenergic Drugs: Effects
Direct acting drugs - act on the receptor directly e.g. adrenaline, dopamine, etc.

Indirect-acting drugs - enhances release of noradrenaline from vesicles e.g. tyramine, amphetamine.

Mixed-acting - cause noradrenaline release + (in higher doses) activate receptor e.g. ephedrine
Direct acting
5 catecholamines in therapeutic use:
Naturally occuring


Indirect & Mixed Acting
Find out indirect acting and mixed acting adrenergic agonists and briefly explain what you found
a2 selective Adrenergic Agonists
Synthetic a2 partial agonist
Main effect of oral clonidine is activation of a2 receptors in the brain results in lowering of BP due to decreased outflow of sympathetic impulses.

Adverse effects include sedation and dry mouth, bradycardia, hypotension.

Old drug for hypertension
ß2 selective Adrenergic Agonists
(US: albuterol)

Treatment for obstructive airway disease (e.g. asthma) require activation of ß2 receptors in lungs which relax bronchial smooth muscle to dilate bronchioles
For airways disorders, ß2 receptor-selective drug is preferable to avoid cardiac side effects of ß1 receptor stimulation.

Direct delivery to the lung is preferable to avoid stimulating ß2 receptor in the skeletal muscle (increased contractility - tremor)
ß2 selective (activate a and ß1 at high doses only)
Direct Acting agonists
Non selective a & ß
Acting adrenergic agonist: amphetamine, tyramine
Acting adrenergic agonist: ephedrine
Selective agonists:
a1 : phenylephrine
a2 : clonidine
ß2 : salbutamol
Mainly released from adrenal medula
Acts on a1, a2, ß1, ß2
heart, ß1: increase HR & inotropy
peripheral, a1 (& a2): increase TPR
muscle, ß2: vasodilation (lower BP)

increase HR & CO, small rise in BP

Lung, ß2: bronchodilation
Major use:
in hypersensitivity, to prevent/treat anaphylactic shock
Restoring cardiac rhythm in patients with cardiac arrest
Prolong action of local anaesthetics by restricting local blood flow

Adverse effects include restlessness, headache, tremor, palpitations
Mainly released from peripheral nerves
Acts mainly on a1 & a2, ß1 (little action on ß2)
heart ß1: increase HR (initially) & inotropy
peripheral a1 (& a2): increase TPR
rising BP causes compensatory baroreceptor reflex to slow HR (via parasympathetic NS).
increase CO & BP
no change in HR
Need blood pressure monitoring to prevent severe hypertension

Limited use: treatment of shock, raising BP
Agonist to both dopaminergic & adrenergic receptors
(Dopaminergic nerves in brain important for movement but i.v. dopamine do not cross blood brain barrier)

Can activate alpha and ß adrenergic receptors

Dopaminergic receptors, distinct from the alpha and beta adrenergic receptors, occur in the peripheral mesenteric and renal vascular beds.
Cardiovascular effect:

Stimulatory effect on the ß1 receptors of the heart, having both inotropic and chronotropic effects.

Very high dose, dopamine activates alpha receptors on the vasculature, resulting in vasoconstriction.

Adverse effects include tachycardia, cardiac arrhythmias, headache, hypertension, nausea, vomiting.
Treatment of severe congestive heart failure, especially with kidney failure - to increase blood supply to heart and kidney (raise urine output)
Treatment of shock - stimulate heart contraction, while increasing blood supply to kidney and other organs (wheareas noradrenaline may reduce blood supply to kidney)
Synthetic drug resembling dopamine, working via mainly ß1 receptors (weak for alpha and ß2): mainly positive inotropic effect (lower dose does not increase heart rate)

Used to increase cardiac output in congestive heart failure.
Increases cardiac output with little change in the heart rate and does not significantly elevate oxygen demands of the myocardium.
major advantage over other sympathomimetic drugs

May increase BP (small) and HR (higher dose)

Other adverse effect are the same as those for adrenaline

US: Isoproterenol
synthetic agonist of ß receptors with insignificant effect at alpha receptors
ß1 increase HR and inotropy
ß2 dilate muscle arterioles (lower BP)
Main effect: increase HR and inotropy with no or small increase in blood pressure
Palpitation, tachycardia, headache, flushed skin
Emergency treatment of bradycardia or heart block, bronchodilator in asthma
Non Selective
Adrenergic Agonists
has structural modification for oral bioavailability and selectivity for ß receptors

formulated for delivery to lungs using metered dose inhaler

additional effect of ß agonists in ashtma: suppression of release of inflammatory chemicals in lung tissue.
Indirect Acting
Tyramine, Amphetamine
enter nerve terminal
transported into vesicles, displace noradrenaline
leakage of noradrenaline from nerve terminals
Fermentation in GIT
monoamine oxidase
Mixed acting
Directly acting: agonist at a and ß receptors
Also indirectly acting: releases stored noradenaline from nerve endings
can be from natural sources or synthetic, is orally active.
Usually increases BP via increase in HR, CO

hypertension, insomnia
Nasal decongestant: sprayed/dropped into congested nostrils - activate alpha receptors in blood vessels of nasal mucosa to cause vasoconstriction which relieve the nasal congestion
MSc Pharmacology & Toxicology
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