Antihypertensive Medications
Drug Class Mechanisms
Diuretics Depletes the body of
Sodium and Reduces
Example: Thiazide Blood Volume by
stimulating Water
excretion
Sympathoplegic Agents Reduces Peripheral
Vascular Resistance,
Central Acting inhibiting cardiac function,
Example: Clonidine increasing venous pooling
in capacitance vessels
Sympathoplegic Agents See above
Beta Blockers
Example: Propanolol
Direct Vasodilators Relaxes SM thereby
dilating resistance vessels
Example: Nitroprusside and increasing
sodium capacitance
Inhibitors of Angiotensin Reduction in PVR and
System Blood Volume
ACE- Inhibitors
Example: Captopril
Route of Admin MOA
Oral Blocks Na/Cl cotransporter
in the DCT of the nephron
thereby inhibiting NaCl
reabsorption.
Oral; transdermal Partial agonist at alpha2-
adrenoreceptors in the
medulla (primary) and
arterioles
Oral; IV Non-selective antagonist
of B-adrenoreceptors (B1
and B2) of the heart and
kidneys
IV Activates guanalyl cyclase
in vascular SM causing an
increase in cGMP levels;
activation occurs by
release of nitric oxide or
direct interaction with the
enzyme
Oral Competitively inhibits ACE
peptidyl dipeptidase on
endothelial cells (enyme
that converts Ang I to Ang
II and also inactivates
Bradykinin)
Pharmacological
Actions/Effects
Inhibits NaCl reabsorption;
Produces diuresis; Promotes
renal excretion of K+ and H+
Prolonged hypotension;
Reduces cardiac output (from
decreased HR, relaxation in
capacitance vessels and
reduced PVR); Decreases
renal vascular resistance and
maintains renal blood flow
Decrease BP and CO; Inhibits
catecholamine-stimulated
renin production; Reduces
sympathetic vasoconstrictor
nerve activity
Vasodilation in both arterial
and venous vessels; reduces
PVR and venous return
Reduces BP; Decreases PVR;
Reduces Ang II levels and
aldosterone secretion;
Increases Bradykinin levels
(vasodiltor)
Major AE/Toxicity
Hypokalemic metabolic
alkalosis; Hyponatremia
Skin reactions
(transdermal); Dry mouth;
Somnolence; Hypertensive
crisis (after stopping use)
Bradycardia; AEs resulting
from exacerbation of other
medical conditions-
bradycardia, cardiac
conduction disorders,
asthma, peripheral
vascular insufficiency, and
diabetes
Excessive hypotension;
cyanide poisoning
(metabolism of the drug);
may also cause metabolic
acidosis, cardiac
arrythmias, and death
Hyperkalemia; Severe
hypotension; Dry cough
Contraindication
Category D in 2nd and 3rd
trimisters/precaution
Antihypertensive Medications
Drug Class Mechanisms
Inhibitors of Angiotensin Reduction in PVR and
System Blood Volume
Angiotensin Receptor-
Blocking (ARB)
Example: Losartan
Ischemic Heart Diseases
Drug Class
Nitrates & Nitrites
Example: Nitroglycerin
Calcium Channel Blockers
Example Verapamil
Route of Admin
Oral
Route of Admin
Oral; Sublingual; Topical
(ointment); Transdermal (patch);
Translingual (spray); IV
Oral; IV
MOA
Inhibition of Ang II type
(AT1) receptor on target
cell membranes
MOA
Metabolized into NO in SM
Cells; NO directly stimulates
action of guanalyl cyclase,
leading to an increase in
intracellular concentration of
cGMP; Dephosphorylation of
MLC and decrease in
intracellular Calcium> SM
Relaxation
Blockade of L-Type calcium
channels located in cardiac and
smooth muscle membranes; Will
bind on the inner side of the
membrane with high affinity to
open channels and inactivated
channels; reduces frequency of
channel opening in response to
depolarization.
Pharmacological Major AE/Toxicity
Actions/Effects
Reduces BP; Decreases PVR Hypoglycemia; Chest
Reduces aldosterone levels Pain; Dry Cough
(especially in those who
were taking an Ace-I
before); severe
hypotension
Contraindictions:
Category D (2nd and 3rd
semester
Pharmacological Actions/ Major AE/Toxicity/
Effects Contraindications
Vasodilation of all types of Orthostatic hypertension;
vessels, especially large veins tachycardia; throbbing
and coronary vessels; Increases headache; tolerance
venous capacitance; Decreases (tachyphylaxis w/ continuous
ventricular preload and workload exposure)
of the heart (decreases hearts
oxygen demand); Reduction of
pulmonary vascular pressures,
heart size, CO, after load and
blood pressure
Decrease in transmembrane Headache; gingival hyperplasia;
calcium current; Long-lasting hypotension
smooth muscle cell relaxation
> vasodilation; Reduces heart
contractility, leading to a
reduction in myocardial oxygen
demand; Decreases SA node
pacemaker rate and AV node
conduction velocity
Heart Failure
Drug Class
Loop or High-Ceiling Diuretics
Drug: Furosemide (Lasix)
Cardiac Glycosides (Digitalis)
Drug: Digoxin
Route of MOA
Administration
Oral; IV Inhibition of Na/K/2CL (NKCC2) co-transporter
in the thick ascending limb (TAL) of the Loop of
Henle
Oral; IV Inhibition of Na/K/ATPase pump in Cardiac
muscle cell membranes; Causes increase in
Sodium; Decreases activity of NCX exchanger
(brings Ca out of cell against concentration
gradient); Increases free calcium; Increases
amount of Calcium taken up by the SR via
SERCA; Increases number of Troponin C
molecules that bind calcium; Increases intensity
of actin-myosin interaction in cardiac muscle
cell sarcomere; Increases force of myocardium
contraction
Pharmacological Actions/ Major AE/Toxicity/
Effects Contraindications
Promotes renal excretion of Hyperuricemia; Hypokalemia;
NaCl, H, K, Mg and Ca; Causes Hypocalcemia;
diuresis; Increases renal blood Hypomagnesemia; Hearing
flow; reduces pulmonary impairment
congestion and left ventricular
filling pressures
Major increase in cardiac Toxic doses of drug- Cardiac
contractility; Decreases SA node arrhythmia, cardiac arrest
rate, refractory period of atrial
muscle, AV node conduction
velocity (but increases refractory
period) and ESV; Small
decrease in refractory period of
the Purkinje muscle; increase
stroke volume
Antiarrhythmic Drugs

Drug Class Route of MOA Pharmacological Actions/Effects Major AE/Toxicity/

Administration Contraindications

Class I IV Inhibition of activated and Reduces cardiac sodium current (I-Na); Neurological symptoms
inactivated sodium channels on Mainly effects Purkinje and ventricular (parethesia; tremor seizures;
Lidocaine cardiac cell membranes cells (no effect on cells with normal etc); hypotension; cardiac arrest;
resting potential); Depression of cardiac dysrhythmia
conduction in depolarized cells; Strongly
increases refractory period in
depolarized cells; decreases pacemaker
activity

Class 2 Inhibition of Beta-adrenreceptors Increases refractory period in

on cardiac cell membranes depolarized cells; decreases SA node
Beta-Blockers rate; increases AV node refractory
Example: Propanolol period; decreases conduction

Class 3 Oral; IV Sodium, Potassium and Calcium
Channels; Blocks IKr; inhibits
Example: Amiodarone alpha and beta adreneregic
stimulation of the heart
Markedly prolongs AP and refractory
period duration in myocardial tissue;
Decreases SA node rate; Increases AV
node refractory period; Causes
peripheral vasodilation
Photosensitivity (upto 75%); AV
block (5%); CHF
Contraindication: Pregnancy/
Lactation Category D

Class 4 See above (IHD) See above see above see above

Calcium Channel Blockers

Example: Verapamil

Hyperlipidemia
Drug Class Route of MOA Pharmacological Actions/Effects Adverse Effects/Toxicity/
Administration Contraindications

Statins Oral Competitive inhibition of HMG-
CoA reductase in hepatocytes
Example: Lovastatin > rate limiting enzyme (first
committed step)
Increase high affinity LDL receptors, fractional Creatine phosphokinase
catabolic rate of LDL and liver extraction of elevations; hepatoroxicity;
LDL precursors from the blood; Reduces LDL rhabdomyolysis
levels; Modestly decreases plasma
triglycerides and induces a small increase in Contraindicatoin: Category X
HDL levels; Decreases protein prenylation by Unsafe in pregnant/lactating
preventing activation of Rho and Rab women
proteins; Significant reduction of new
coronary events and atherothrombotic stroke.
Hemostatic Disorders

Drug Class Route of Administration MOA Pharmacological Actions/ AEs/Toxicity/

Effects Contraindications

Thrombolytics IV Catalyzes formation of plasmin Breakdown of hemostatic Hemorrhagic stroke; bleeding;

from plasminogen that is bound thrombi and target hemorrhaging at virtually any
Example: Alteplase to fibrin thromboembolic site; CV complications

Recombinant Human tissue

Plasminogen Activator (t-PA)

Hemostatics IV Functions as a cofactor for Stimulates production of factor Factor VII Inhibition disorder
factor IXa which converts Factor Xa; Stimulates coagulation
Example: Antihemophilic X into the active form, Factor Xa cascade
Factor Recombinant

Recombinant Human Factor

VII