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Adrenergic

Drugs

Alpha 1
Alpha 2
Blood vessels
Pre-synaptic nerve
terminals: inhibit NE
Eyes

Bladder

Male sex organ
Prostate

RAR Pharm 1 Chart C/o 2017

Beta 1
Primarily in the
heart



Beta 2
Skeletal
muscle vessels
Bronchi, lung
Uterus in
delivary


1 and 1
2 and 2
Excitation (constriction) Inhibition (relaxation)


Alpha Agonist

Drug Name

3 (brown fat)

Norepinephrine
Alpha 1, Alpha 2, Beta 1
VC of BV in skin/mucosa
Systemic VC TPR BP

NE induces 1 + 1 stimulate VC
baroreflex will in return BP

thermogenesis

Phenylephrine

Epinephrine
Alpha 1, Alpha 2, Beta 1, Beta 2
VC of BV in skin/mucosa
dose epi: BP (stimulate 2 to relax
skeletal muscles, tachycardia)
dose epi: BP (stimulates 1 to
contract BV; same effect as NE)
At Epi, 1 + 1 stimulate VC
baroreflex will in return BP
At Epi, 2 stimulate VD baroreflex
will in return BP

Clonidine

Receptor affinity Alpha 1 selective

Alpha 2 selective

Mechanism

Functions similarly to an anti-androgenic drug (because it stops NE)

Effect
Therapeutic uses
Notes

Used in low doses to activate receptors blood vessel constrictions. May


activate receptors are much higher concentrations.
Arterial VC with IV infusion

BP, transient VC followed by prolonged hypotensive response


sympathetic outflow from the CNS
Restore BP during anesthesia, hypotensive emergencies or alter overdose of Antihypertensive, antidepressive
an antihypertensive medication
Could be dangerous if used long term because 2 has negative feedback
Neo-synephrine: nasal spray to increase BP in acute BP situations
that blocks the release of NE which prevents the sympathetic response.


Beta Agonist

Drug Name
Doubutamine
Receptor affinity Beta 1 selective
Mechanism
1 works mainly in the heart to constrict thereby
HR
Effect
Contractibility HR
Therapeutic uses Severe congestive heart failure

Notes

Best medication for heart because theres little


side effects on the lungs (safe for asthma pts)

Isoproterenol
Beta 1, Beta 2 non-selective
1 works in the heart to constrict while 2 works
to dilate blood vessels and bronchi
Contractibility HR CO
Vasodilation = diastolic BP = TPR
Torsades de points: ventricular trachycardia that
results in sudden BP
Cardiac arrest of complete heart block
Use of isoprenaline for asthma pt is not
recommended because the drug will have its
effects on the heart as well

Albuterol
Beta 2 selective
2 inhibits (relaxes) the lungs so the bronchi are
open
Bronchodilator
Asthma, long-term treatment of obstructive
airway disease, acute bronchospasm
It would be beneficial if albuterol can be
administered locally to avoid interaction with 2
receptors on skeletal m, pancreas, liver

RAR Pharm 1 Chart C/o 2017


Alpha antagonist
Blocking receptors main effect is to BP

Drug Name
Phentalomine
Phenoxybenzamine
Prazosin/Terazosin/Doxazosin
Yohimbine
Receptor affinity Alpha Non-selective
Alpha Non-selective
Alpha 1 selective
Alpha 2 selective
Mechanism
Competitive binding (less toxic)
Non-competitive binding (toxic)
Blocks 1 to prevent VC
Blocks 2 so theres no () feedback
Effect
-Unopposed receptor: VD,
-Unopposed receptor: VD,
TPR BP
BP HR

progressive TPR, CO hypotensive progressive TPR, CO hypotensive
Side effect: postural hypotension
response to Epi
response to Epi
sympathetic effect and poteniate
(when
y
ou
g
et
u
p
q
uickly,
y
our
NE release from nerve endings
-Blocked 2 receptor: NE (no
-Blocked 2 receptor: NE (no
blood
p
ressure
d
rops)
a
nd
s
yncope

feedback), tachycardia
feedback), tachycardia
Therapeutic uses Reversal of soft tissue anesthesia,
Pheochromocytoma, preparation for Essential HTN (greater therapeutic
In the past: erectile dysfunction
pheochromocytoma induced HTN
surgery
utility than phenoxybenzamine)
Notes
Doesnt effect the absorption of LA
More toxic effect because no matter Prazosin: T: 2-3 hrs, compliance

but it blood flow to allow the LA to how much endogenous ligand is
Terazosin: T 12 hrs. Bioavailability
released, the drug will remain bound Doxazosin :T 10-20 hrs (best one)
be flushed out of the soft tissues


Beta antagonist

Drug Name
Propranolol
Atenolol/Metoprolol/Esmolol/Acebutolol
Third generation drugs
Receptor affinity Beta non-selective
Beta 1 selective
Combination of antagonism + CV effects
Mechanism

Blocks binding to which will usually act to
Blocks binding to 1 which will usually act to
constrict the heart
constrict the heart
Effect
BP HR contractibility frequency. NO
BP HR contractibility frequency. NO
VD actions by: 1 and 1 antagonism, 2
postural hypotension
postural hypotension
agonist, production of nitric oxide = mediated
2+
VD, Ca entry blockade, K+ channel opening,
anti-oxidant functions
Therapeutic uses HTN, ischemic heart disease, post MI CHD,
HTN, ischemic heart disease, post MI CHD, cardiac
cardiac arrhythmias
arrhythmias
Notes
Contraindicated for pts with bronchosplastic
Less adverse effects than non-selective agonist

disorders because B2 is needed for bronchi
relaxation (ex. Asthma) and diabetes

*NOTE: when thinking about increasing or decreasing blood pressure think of VESSELS. 1 receptor is in charge of blood vessels and it EXCITED (constricts). 2 is in charge of blood vessels and it INHIBITS (dilates). So when
you want to DECREASE BP then you have to BLOCK (blocks constriction = blocks increase in BP) OR you have to have a 2 agonist. If you want to INCREASE BP then you have to BLOCK 2 or have an agonist. Also
blockers act by blocking the action of B1 in the heart. B1 when stimulated by NE of the sympathetic system will increase heart rate and blood pressure. When you BLOCK this response then you are decreasing heart rate
and contractibility thus reducing the persons risk for a recurrent heart attack. blockers are used for patients with HTN or post MI or arrhythmia
**NOTE: alpha antagonist will prevent binding of the endogenous ligand to the alpha receptors making MORE ligands available to bind to beta receptors. The result is a in BP because they will mostly bind to 2 which
causes VD. They do have some action on beta 1, but baroreflex corrects that, so what we see in actually a decrease in BP.

Mixed acting

Drug Name
Ephedrine
Receptor affinity Alpha 1, Alpha 2, Beta 1, Beta 2
Mechanism
Acts in two ways: 1) directly at the receptor as and agonist) and 2)
releases mediators in the synapse
Effect

Therapeutic uses
Notes


Indirect acting adrenergic agonist

Drug Name
Receptor affinity
Mechanism
Effect
Therapeutic uses
Notes

Amphetamine
Not selective
Stimulation of the mediator synthesis and release
CNS stimulant
ADHD, recreational drug abuse avoid using VC
Readily develops tolerance to the CNS stimulant
effects, appetite suppression and mood elevation

Metaraminol
Alpha 1, Alpha 2, Beta 1, Beta 2



Cocain
Not selective
Inhibition of mediator uptake





Indirect Acting Adrenergic Antagonists
Clonidine/Guanabenz -2 Agonists (block negative feedback)
Reserpine

Disruption of neurotransmitter vesicles (NT degraded in cell)

Guanethedine

Decrease release of sympathetic transmitters

-Metildopa

Decrease transmitter production

6-Hydroxydopamine

Kill dopaminergic neurons

RAR Pharm 1 Chart C/o 2017

MAO inhibitor
Not selective
Inhibition of the mediator inactivation


Lots of side effects but can find homeostasis

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