Check list of common cardiac drugs

Drugs Main effects Mechanism Sites of action

abciximab anticoagulant stops monoclonal antibody platelets
platelet activation to fibrinogen receptors
amiloride (combination potassium sparing plasmalemma sodium kidney (distal
with frusemide is diuretic & chloride channels tubules)
frumil)
amiodarone class III anti-arrhythmic prolongs action myocardium
potential duration
aspirin anticoagulant stops COX inhibitor, blocks platelets
platelet activation TXA2 synthesis
atropine (sometimes parasympatholytic, blocks muscarinic pacemaker cells
used to stop vagus increases heart rate AcCh receptors (sino-atrial node)
bradycardia)
captopril reduces arterial blood ACE inhibitor relaxes vascular
pressure smooth muscle
clopidogrel anticoagulant stops blocks ADP receptor platelets
platelet activation
digitalis and ouabain increase cardiac block Na / K ATPase all tissues, but the
contractility, delay AV raising intracellular Na/Ca exchanger is
node triggering sodium, then calcium mainly in heart
dipyridamole (often coronary vasodilation inhibition of adenosine coronary
used for X-ray uptake vasculature
imaging)
furosemide (= diuretic plasmalemma sodium kidney (loop of
frusemide) & chloride channels Henle)
isoprenaline (and other increase cardiac beta agonist raises many tissues
adrenaline analogues) contractility cyclic AMP
losartan reduces arterial blood angiotensin AT1 relaxes vascular
pressure receptor blockade smooth muscle
lovastatin reduces blood cholesterol HMG-CoA reductase liver
levels inhibitor
morphine pain relief (mainly) opiate receptors brain
nitroglycerine (and reduce cardiac work load metabolised to NO relaxes vascular
many other organic smooth muscle
nitrates)
propranolol reduces cardiac beta blocker lowers many tissues
contractility, class II anti- cyclic AMP
 arrhythmic
quinidine, novocaine class I anti-arrhythmics delay recovery of myocardium
and other local sarcolemma sodium
anaesthetics channels after AP
spironolactone (usually reduces diuretic aldosterone antagonist kidney (distal
added to other potassium losses tubules)
diuretics)
urokinase dissolves blood clots activates plasminogen blood clots
(streptokinase is (fibrinolytic) to plasmin (protease)
cheaper but antigenic)
verapamil, nifedipine reduce cardiac work load, block sarcolemma myocardium; relax
and other class IV anti-arrhythmic calcium channels vascular smooth
dihydropyridines muscle
warfarin anticoagulant blocks -carboxy liver
glutamate synthesis
vit. K antagonist

Vasoactive peptides (all of these use seven transmembrane helix receptors)

peptide name produced by actions

adrenomedullin everywhere vasodilation
angiotensin renin, ACE (proteases) vasoconstriction
atrial natriuretic right atrium stretch increased water and sodium losses by kidney
B-natriuretic ventricular muscle as above
C-natriuretic vascular endothelium as above
bradykinin kallikrein (protease) vasodilation, increased vascular permeability
endothelin vascular endothelium vasoconstriction, bronchoconstriction
vasopressin posterior pituitary increases renal water retention
VIP parasympathetic nerves vasodilation (salivary glands)

other vasoactive substances

name produced by actions

adenosine all working tissues vasodilation
adrenaline adrenal medulla vasodilation () predominates
aldosterone adrenal cortex sodium retention by kidney
histamine mast cells both constriction & dilation (receptors)
leukotriene LTC4 leukocytes vasoconstriction, bronchoconstriction
noradrenaline sympathetic nerves vasoconstriction () predominates
nitric oxide vascular endothelium vasodilator via cGMP
prostacyclin PGI2 vascular endothelium vasodilation, prevents clotting
prostaglandin PGE1 / E2 macrophages both constriction and dilation (receptors)
thromboxane TXA2 platelets vasoconstriction, promotes clotting

drug name type actions

levosimendan calcium sensitizer enhances troponin Ca++ binding & opens
vascular ATP-sensitive K+ channels
cytokine inhibitor anti-inflammatory
bosentan endothelin receptor antagonist
ghrelin growth hormone releaser
nesiritide natriuretic peptide increases salt and water excretion
thiorphan neutral endopeptidase inhibitor blocks degradation of bradykinin & ANP
eplerenone selective aldosterone receptor blocks aldosterone actions in kidney and in
antagonist (SARA) cardiac muscle (anti-fibrosis)
omapatrilat vasopeptidase inhibitor blocks both angiotesin II formation, and the
degradation of bradykinin and ANP
vasopressin antagonist blocks V2 receptors in collecting ducts