Class

Adrenergic Agonists

Drug

Mechanism

Uses

Epinephrine

a1, a2, b1, b2

anaphylactic shock,
cardiac arrest,
reduces bleeding
during surgery

Norepinephrine

a1, a2, b1

Dopamine

B1, a1

Dobutamine
Oxymetazoline,
Phenylephrine
Albuterol,
Terbutaline,
Salmeterol

b1

a2

Ritodine
Amphetamine

b2
NE release
NE uptake
blocker

Ephedrine,
pseudoephedrine

a1, NE release

Metoprolol, Atenolol

b1

Propranolol

b1, b2
b1, b2 blocker,
partial agonist
b1, b2

Pindolol
Timolol

Adrenoreceptors

b2

Clonidine

Cocaine

Adrenergic Blockers

a1

hypotension, shock
cardiogenic and
septic shock, heart
failure
cardiogenic shock
nasal, ocular
decongestion
asthma
decreases
sympathetic outflow
from CNS hypertension
premature labor
narcolepsy, ADD
LA
nasal decongestion
hypertension,
angina
same as above
hypertension
hypertension, AMI

Doxazosin, Prazosin,
Terazosin,
a1
Tamsulosin

hypertension

Phentolamine
Lebetalol

hypertension
hypertension

a1, a2
a1, b1, b2
a1

vasoconstriction,
increase BP
pupil dilation
constrict urinary
bladder

a2

decrease NE release
and therefore
sympathetic outflow

b1

increase HR,
contractionf force,
AV conduction

renin secretion

b2

relaxation of
bronchiol smooth
muscle
Glycogenolysis
Uterus relaxation

Muscarinic Receptor
Agonists

**generally reduce
intraocular pressure
in glaucoma,
increase motility in
GI and urinary tracts
stimulates
peristalsis after
abdominal surgery
used in urinary
retention post op
patients with
Xerostomia to
increase salivary
secretions; treat
patients with
glaucoma

Bethanechol

Pilocarpine

Cholinesterase
Inhibitors

Cevimiline

M3 agonist

Endrophonium

rapid renal
binds reversibly
clearance, brief
to AChE
duration of action

Muscarinic Receptor
Antagonists

Tacrine, Donepzil

higher affinities and

binds reversibly partition into lipids,
to AChE
used to treat
Alzheimers

Physostigmine,
Neostigmine

carbamate
inhibitors
essentially, bind
to AChE and
hydrolyzed at
slow rate
(carbamylated
enzymes takes
hours to cleave)

Dicyclomine

Muscarinic
receptors

Glycopyrrolate

Muscarinic
receptors

Pirenzepine
Oxybutynin,
Tolterodine,
Darifenacin,
Solifenacin,
Trospium
Ipratropium,
Tiotriopium
Tropicamide
Benzotropine

Ganglionic Blockers

Trimethaphan

Sodium
nitroprusside

M1 receptors

relaxes intestinal
smooth muscle in
IBS
inhibit excessive
salivary and
respiratory tract
secretions
reduces gastic acid
secretion, blocks M1
on paracrine cells
more selective on
urinary bladder reduces the 4 major
symptoms of
overactive bladder
administered to
patients with
destructive lung
diseases
pupillary dilator
Parkinson's

blocks nicotinic
receptors at
block
autonomic ganglia
sympathetic and not at the NMJ
parasympatheti used in
c ganglia
hypertensive
emergencies over
ganglionic blockers

Ganglionic Agonists

increases BP, HR;

enters the brain,
causing alertness,
vomiting, tremors

Nicotine

Nicotine

activitates
nicotinic
receptors at
NMJ; activates P
and S ganglia

curare

Block action of motor weakness

ACh at nicotinic progresses to total
receptor site
flaccid paralysis

Depolarizing
Neuromuscular
Blockers

Succinylcholine

causes persistent
receptor
Binds to and
stimulation;
actiavtes
Succinylcholine is
muscle nicotinic hydrolyzed primarily
receptors
by
butyrylcholinesteras
e in plasma

Drugs for Glaucoma

Prostaglandin PGF2a

increases outflow
through uveoscleral
pathway

Latanaprost,
Travoprost

fewer side effects

and long duration of
action

B receptor agonist ;
Timolol, Levobunolol

most commonl used

; decrease
production of AH by
reducing secretion
as well as reducing
blood flow

Nicotinic Receptors
Agonists

Competitive
Neuromuscular
Blockers

a2 receptor
agonists;
alpraclonidine
Carbonic anhydrase
inhibitors;
dorzolamide,
brinzolamide

reduces AH
production
inhibit carbonic
anhydrase II in
ciliary body
epithelium

contraction of cilary
muscle, facilitates
outflow of AH

Muscarinic agonists;
Pilocarpine

Drugs used in
Asthma

Beta agonists

Epinephrine,
Salbutamol,
Salmeterol

agonist of B2
receptors on sm causes bronchiol sm
ms cells, raises ms to relax
cAMP levels
adenosine
antag, PDE
inhibitory, NE
release
m3 receptor
antagonist

Methylxanthines

Theophylline

Muscarinic antagonists

Ipratropium

Leukotriene receptor
antagonists

Zafirlukast,
montelukast

antagonist of
LD4 receptor

Release Inhibitors

Cromolyn,
Nedocromil

hyperpolarize
cells and
not bronchodilators
prevent release

Prednisone,
Beclomethasone

reduce number
of inflammatory
not bronchodilator
cells and
mediators

Acetazolamide

Works at the
PCT - Inhibits
carbonic
anhydrase
prevent HCO3formation and
more HCO3excreted

Best drug to cause

hypokalemia; used
to reduce
intraocular pressure

Furosemide,
Bumetanide

Work at LoH;
Inhibits luminal
co-transport of
Na, K, Cl;
therefore these
all get secreted

Drug must be in
lumen to work; It is
useful if one has
hyperkalemia

Corticosteroids

Bronchodilator

Diuretic Drugs

Carbonic Anhydrase
Inhibitors

Loop Diuretics

Thiazide Diuretics

K+ sparing Diuretics

Osmotic Diuretics

Works at DCT;
Reduces reabs
Hydrochlorothiazide, of Na, Cl; more
Indapamide
Na, K, H and Cl
lost, HCO3
retained
Works at DCT;
reduces Na-K, H
exchange at
Spironolactone,
DCT; leads to
Amiloride
increased Na
loss, K and H
retention

Mannitol

PCT, DLoH;
prevent water
reabs at these
two locations,
ADH antagonists
leading to
used in chronic
increased water
SIADH
secretion; ADH
antagonists
prevent cAMP
formation

Antihypertensives

Diuretics

Beta Blockers

ACE inhibitors

Spironolactone is an
aldosterone
competitive
antagonist

reduces Na/H2O
reabs at DCT,
Hydrochlorothiazide,
reduce plasma
indapamide,
volume, reduce
chlorthalidone
venous return,
reduce CO (BP)
Blocks B1,
increasing TP;
block B1 which
Metoprolol, Atenolol
effects B1
(Look for "lol" in
receptors in
suffix)Preferably not
heart and reninB2 involvement
secreting cells,
therefore you
get lower renin
Captopril, Enalapril, prevent the
Ramipril, Perindopril formation of
(look for the "pril"
angiotensin II,
suffix"
lowering BP

ARBs (angiotensin
receptor antagonists)

irreversibly bind
to AT1 receptors
Losartan, Valsartan,
(subtype of ANG about as good as
Olmesartan (end
II receptors)
ACEi
with "sartan" suffix)
reducing effects
of ANG II

Calcium Antagonists

Amlodipine,
vascular smooth
Nifedipine,
muscle, cause it
Diltiazem, Verapamil to relax

Direct Vasodilators

Hydralazine,
Minoxidil

a2 agonists

Clonidine,
Methyldopa

Direct Renin Inhibitor

Aliskiren

Inhibits renin,
lowering BP

Decreasing Preload

Diuretics, nitrates

Reduce CO;
Diuretics reduce
volume, venous
mainly reduce the
return; nitrates
symptoms
increase
capacitance,
reduce VR

Decreasing Afterload

ACEi, ARBs
decrease ANG II
effect lowering
ACEi, ARBs,
TPR and BP;
Hydralazine, Nitrates
Hydralazine and
Nitrates are
vasodilators

not useful alone as

they increase HR
and Na retention
Often used only
short term

Drugs to treat Heart

Failure

Digoxin inhibits
Na-K exchange,
this increases
intracellular Na,
Digoxin, Milrinone, B
increasing NaIncreasing Contractility agonist - cardiac
Ca exhange,
glycosides
increasing
intracellular Ca,
increasing
contractility

digoxin causes
slower
depolarization,
faster
repolarization, can
cause arrythmias

B agonists

Phosphodiesterase
Inhibitors (PDE)

Epi, NE,

B agonsists

significant inotropic
response for a short
term

Dobutamine

activates
several
adrenergic
receptors,
releasing NE
from
sympathetic
nerves

dose dependent, but

positive inotropic
action occurs as a
result of B1 activity

Milrinone

Inhibit cAMP
phosphodiestera
se, the enzyme
that activates
cAMP;

Drugs to treat
Regional Ischemia

B Blockers

Calcium Channel
Blockers (CCB)

Reduces HR,
Meotoprolol, Atenolol
contractility,
("Prefix is LOL)
afterload,

Verapamil,
Diltiazem, 'pines

Block Ca
channels (sinus
node, AV node,
myocardium,
peripheral
vessels

compete with epi

and NE

Reduce HR,
afterload (BP), have
a negative inotropic
effect (contractility)

Clinical

a1 blockers decrease BP
a1 agonists increase BP
a1 agonists dilate pupils
a blockers used to treat
urinary retention

Side Effects

a2 agonists decrease
sympathetic outflow,
good to treat
hypertension
b1 agonists help treat
heart failure; b1 antags
can treat hypertension,
tachycardia; selectibe b1
can help treat asthma
patients
b blockers decrease renin
formation and ultimately
decrease BP
b2 agonists used to treat
asthma
b blockers can prevent
breakdown of glycogen
b2 agonists can treat
uterie hypermotility to
prevent premature labor

less side effects than

pilocarpine

urinary retention,
constipation, blurred
vision, no sweating, toxic
psychosis

Ganglionic blockade (fall

in BP), blockage of vagal
resopnse, Histmaine
release
used in anesthesia to
obtain skeletal muscle
relaxation, orthopedic
procedures, facilitate
tracheal intubation,
prevent trauma during
electroshock therapy

best one

release K+ rapidly from

intracellular sites causing
hyperkalemia

these drugs and ChE

inhibitors have lots of
side effects are are
seldom used

must be inhaled or
systemic to get to site of
action

less effective in asthma

than b2 agonists
less effecitve in asthma
than b2 agonists
oral; good for aspirin
induced asthma; less
effective in asthma than
b2

steroid sparing

inhaled only, may cause

irritation
systemic initially, topical
later; use lowest dose
possible

rarely used as a diuretic;

more commonly used to
treat glaucoma

these are used to reduce

plasma volume and CO

steroid sparing

END WITH
KAST!

these are used to reduce

plasma volume and CO

rarely used alone; used to contraindication with

treat low K
digoxin

over admin may lead to

hyperkalemia,
hypernatremia

intiially CO drops and TPR

increases, but then after
4 weeks, TPR drops and
CO increases (BP still
low)

Differs from other PDE

inhibitors that increase
cAMP but not cGMP,
leading to PKA
phosphorylating Ca
channels in the heart,
enhancing Ca influx and
an increase in inotropy

Pindolol will not reduce

HR

Reduced max exercise

tolerance, never
prescribe BB to people
with asthma as they
cause
bronchoconstriction, cold
hands, bad dreams,

SE show up in other
pines have a higher
smooth muscle affinity for smooth muscle
constipation and urinary
than for cardiac muscle
retention