Drugs
Alpha
1
Alpha
2
Blood
vessels
Pre-synaptic
nerve
terminals:
inhibit
NE
Eyes
Bladder
Male
sex
organ
Prostate
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
Alpha 2 selective
Mechanism
Effect
Therapeutic
uses
Notes
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
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
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
Guanethedine
-Metildopa
6-Hydroxydopamine
MAO
inhibitor
Not
selective
Inhibition
of
the
mediator
inactivation
Lots
of
side
effects
but
can
find
homeostasis