This document provides a checklist of common cardiac drugs, their main effects, mechanisms of action, and sites of action. It also lists various vasoactive peptides and substances produced in the body that can cause vasoconstriction or vasodilation, as well as newer drug therapies for heart conditions. The lecture notes were prepared by Mark Fredderick R. Abejo and cover key aspects of the cardiovascular system and its pharmacology.

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

2. Lecture Notes on Cardiovascular System
Prepared By: Mark Fredderick R Abejo R.N, MAN
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 cardiac muscle
antagonist (SARA) (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