ACE Inhibitors

decrease angiotensin II, inhibit degradation of bradykinin, and
decrease aldosterone

Angiotensin-Receptor Blockers (ARB's)

decreases activation of AT1 receptor and the effects of angiotensin II

Beta Blockers

decreases hypertension and activation via sympathetic nervous system

Thiazide

block reabsorption of sodium in the kidney, which decreased water reabsportion

Loop Diuretics

block sodium and water reabsorption

Inotropic Drugs

inhibits Na/K pump, which causes an increase in intracellular sodium

Beta-Adrenergic Agonists

increase Ca+ channels by increasing cAMP

Phosphodiesterase (PDE) Inhibitors

increase cAMP leading to increased Ca+2 and positive inotropic effect

Aldosterone Antagonists

prevent sodium retention, myocardial hypertrophy and hypokalemia

Class I Antiarrhythmics

slows depolarization rate by blocking voltage-gated sodium channels

Class II Antiarrhythmics

treat slows ventricular rates by blocking beta receptors and reduce
strength of heart�s contractions

Class III Antiarrhythmics

treat life threatening ventricular arrhythmias by slowing repolarization

Class IV Antiarrhythmics

treat supraventricular arrhythmias with rapid heart rate

Organic Nitrates

inhibits coronary vasoconstriction or spasm

Calcium Channel Blocker

block L-voltage calcium channels deceasing cytosolic calcium and
muscle contraction

Sodium Channel Blocker

inhibits sodium current decreasing action potentials and indirectly
decreasing calcium concentration in cells

Potassium-Sparing Diuretics

inactivates the steroid receptor and prevents Na+ reabsorption and K+
and H+ secretion

Cholesterol Absorption Inhibitors

inhibit cholesterol absorption in the small intestine

Bile Acid Sequestrants

prevents reabsorption of bile salts and cholesterol in GI tract

Nicotinic Acid

inhibits triglyceride lipase and stimulates lipoprotein lipase,
decreasing triglycerides

Fibric Acid Derivaties

inhibits breakdown of fat into triglycerides in adipose tissue

HMG-CoA Reductase Inhibitors

inhibit the rate limiting enzyme necessary for cholesterol synthesis