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8/6/2019 Report in Pharma
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ADRENERGICPHARMACOLOGY
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Phyllis Schweitz
1960s
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230/160mm hg
headache
nausea
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PHENTOLAMINE
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SYMPATHETIC TRANSMISSION
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Dopa decarboxylase
Dopamine hydroxylase
MAO
MAO
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SYMPATHETIC STIMULATION
` stimulates heartbeat
` raises bloodpressure
` dilates the pupils
` dilates the tracheaandbronchi
` stimulates the conversion ofliver glycogen intoglucose
` shunts bloodaway from the skin and viscera to theskeletal muscles, brain, and heart
` inhibits peristalsis in the gastrointestinal (GI) tract
` inhibits contraction ofthe bladderandrectum
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SYMPATHOMIMETIC DRUGS
Substances that mimic the effects ofthe sympathetic
nervous system
Mimic the effects ofits neurotransmitters
Norepinephrine
Epinephrine Dopamine
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CLASSIFICATION OF
SYMPATHOMIMETIC DRUGS
DIRECT ACTING
Act on one ormore ofthe adrenergic receptors
INDIRECT ACTING
Increase availability ofepinephrine or norepinephrine
Releasingordisplacing NE from the storage vesicle(amphetamine)
Blocking the entry ofNE back into the sympathetic
neurons (cocaine) Blocking the metabolizing enzymes MAO and COMT
MIXED ACTING
Indirectly release norepinephrine anddirectly act on thereceptor (ephedrine)
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CLASSIFICATION OF
SYMPATHOMIMETIC DRUGS
DIRECT ACTING
Act on one ormore ofthe adrenergic receptors
INDIRECT ACTING
Increase availability ofepinephrine or norepinephrine
Releasingordisplacing NE from the storage vesicle(amphetamine)
Blocking the entry ofNE back into the sympathetic
neurons (cocaine) Blocking the metabolizing enzymes MAO and COMT
MIXED ACTING
Indirectly release norepinephrine anddirectly act on thereceptor (ephedrine)
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Dopa decarboxylase
Dopamine hydroxylase
MAO
MAO
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HYPERTENSIVE CRISIS
Monoamine Oxidase
Involved in oxidative deamination of
monoamines (catecholamines) rendering themunable to exert theirfunction
Monoamine oxidase inhibitors (MAOIs)
Prevent deamination followingreuptake of
catecholamines intopresynaptic terminals.
Therefore, more catecholamine accumulates in
presynaptic vesicles forrelease during each
action potential.
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MECHANISM OF HYPERTENSIVE CRISIS
tyramine
Adrenergic nerve terminals
Neural cytoplasm
Displace transmitters from their storage
Via bloodstream and BBB
If MAO is inhibited by MAOI
Via NET
Via VMAT
The mass transfer of norepinephrine from its vesicular storage space
into the extracellular space can precipitate the hypertensive crisis.
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MAOI + TYRAMINE
MAOi intensifies the effect ofTyramine Increase
in bloodpressure
This occurs because ofincreasedbioavailability
oftyramine and increasedavailability of
cathecholamines at the synaptic cleft
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PHENTOLAMINE
Phentolamine is areversible, nonselective a-
adrenoceptor antagonist.
Competitive antagonist at both 1 and 2
receptors
Reduces TPR (total peripheral resistance)
Phentolamine was the ideal agent foruse inintroductory case, because it blocked the a-
adrenergicmediated vasoconstriction that
caused hypertension.
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PHENTOLAMINE ADVERSE
EFFECTS
postural hypotension, flushing, headache
reflex tachycardia
baroreflex mechanism
presynaptic 2 receptorantagonismmay lead to enhanced NE release from
sympathetic nerves
triggers arrythmias andanginal pain in patientsw/ decreased coronary perfusion
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BETA ADRENERGIC BLOCKERSBETA ADRENERGIC BLOCKERS
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DRUGS USED INDRUGS USED IN
HYPERTENSIVE CRISISHYPERTENSIVE CRISIS
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DRUGS USED TO MANAGE
HYPERTENSIVE
Enalaprilat
ACE-inhibitor with arapidonset ofaction and longduration ofaction.
Onset/duration:W
ithin 15 to 30minutes/12-24 hr
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Esmolol
Beta-1 selective blocker. Rapidly
metabolizedby blood esterases (short half-life ~ 9 minutes) and total duration ofaction
~ 30 minutes. Its effects begin almost
immediately.
Onset/duration:1-5 min/15-30 min.
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Fenoldopam mesylate
Fenoldopam is arapid-acting vasodilator.
It is an agonist forD1-like dopamine receptorsandbinds with moderate affinity to 2-
adrenoceptors.
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Hydralazine
Direct arteriolar vasodilator with
little or no effect on the venous
circulation.
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Labetalol
Combinedbeta-adrenergic (B1and B2) andalpha-adrenergic
blocker.
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Nicardipine
Dihydropyridine calcium channelblocker.
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Nitroglycerin
Primarily a venous dilator (lesser
degree - arteriolardilator). It may be most
useful in patients with symptomatic
coronary disease and in those with
hypertension following coronary bypass.Drugofchoice for hypertensive
emergencies with coronary ischemia.
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Sodium nitroprusside
Arteriolarand venous dilator.Considered tobe the most effective
parenteral drugformost hypertensive
emergencies (except myocardial ischemia
orrenal impairment). It dilates both
arteries and veins, and it reduces
afterloadandpreload.
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RESERPINE
Adrenergic Neuron Blocker
Inhibits the function ofpostganglionic adrenergic
neurons
an alkaloid extractedfrom the roots ofan Indian
plant, Rauwolfia serpentina
Effect: Lowers bloodpressure by a combinationofdecreased cardiac output anddecreased
peripheral vascularresistance
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MECHANISM OF ACTION
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GUANFACINE
Centrally Acting Sympathoplegic Drugs
orally active antihypertensive agent
whose principal mechanismofactionappears tobe stimulation ofcentral 2 -
adrenergic receptors.
Effect: This results in adecrease inperipheral vascularresistance anda
reduction in heart rate.
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