Drugs acting on the

cardiovascular system
By
Dr. Fazlullah Khan
 Cardiovascular system:

(System comprises of heart and blood vessels)

▪ Heart has the property of Auto rhythmicity
means generate its own electric impulse.
▪ Heart is supplied with both sympathetic and
parasympathetic nerve.
▪ SA node called pacemaker.
▪ Function of heart= Delivery of blood, O2 and
nutrients
• Factors affecting heart rate=
• Autonomic activity
• Age
• Baroreceptors
• Physical activity
• Emotion
• What is normal blood pressure?
(120/80 mmHg)
Common Heart disorders:
➢Heart failure
➢Angina
➢Cardiac arrhythmias
➢Hypertension
 Antianginal Drugs

❑Angina:
Angina, also known as angina pectoris, is chest pain or
pressure, a symptom of coronary heart disease, usually
due to insufficient blood flow to the heart
muscle (myocardium).
Angina is usually due to obstruction or spasm of
the arteries that supply blood to the heart
muscle. Other causes include anemia, abnormal
heart rhythms, and heart failure. The main
mechanism of coronary artery obstruction
is atherosclerosis as part of coronary artery
disease.
❑Atherosclerosis:
▪ Disease of coronary arteries.
▪ Ischemic heart disease.
Atherosclerosis: in which the wall of
the artery develops abnormalities,
called lesions. These lesions may lead to
narrowing due to the build-up of atheromatous
plaque (Fat, Cholesterol).
• Angina is characterized by sudden, severe
chest pain radiating to Neck, Jaw, Arm (left).
❑Angina is caused by:
• Decrease oxygen in coronary blood flow.
• Spasm of vascular smooth muscles.
• Obstruction of blood vessels by Atheroma.
During angina:
Imbalance between oxygen demand and supply

All these conditions lead to deterioration of

heart function and ultimately cause arrhythmia
and then death.
Coronary blood flow inversely proportional to
coronary vessels resistance.
The Antianginal drugs work via:
Lower oxygen demand of heart by affecting
blood pressure, venous return

Change in life style is mandatory (smoking, junk

foods)
Risk factors for angina:
HTN, Diabetes, Hyperlipidaemia, life style
 Types of angina
❑ Stable angina:
Chest pain that happens when your heart muscle needs more oxygen than usual but
it's not getting it at that moment because of heart disease.
▪ Effort induced angina
▪ Characterized by burning, heavy or squeezing chest pain.
❑ Unstable angina:
When you get angina symptoms while doing very little or resting.
▪ Chest pain with increase intensity and frequency
❑ Prinzmetal angina:
Vasospastic angina is also known as prinzmetal angina, variant angina or coronary
artery spasm. It develops when a coronary artery supplying blood and oxygen to your
heart goes into spasm and suddenly narrows.
▪ Uncommon pattern
▪ Coronary artery spasm
▪ Not related with work out.
Classification of Antianginal drugs
1. Nitrate:
Short acting:
▪ Glycerine Trinitrate
▪ Isosorbide dinitrate
Long acting:
▪ Isosorbide dinitrate (oral)
▪ Isosorbide mononitrate
2. β-blockers:
▪ Propranolol
▪ Metoprolol
▪ Atenolol
3. Calcium channel blockers:
▪ Verapamil
▪ Diltiazem
▪ Amlodipine
4. Potassium channels openers:
Nicorandil
5. Sodium channel blockers:
Ranolazine
 Organic Nitrates
• Examples:
• Nitro-glycerine
• Isosorbide dinitrate
• Isosorbide mononitrate

MOA:
1. They are vasodilators
2. They are converted into nitric oxide which is a vasodilator.
3. They are converted into nitric oxide by;
Glutathione-s-transferase
Aldehyde reductase
4. Nitric oxide activates vascular guanylyl cyclase
5. Guanylyl cyclase causes increase synthesis of cGAMP
6. cGMP cause dephosphorylation of protein kinase
7. This prevent interaction of actin and myosin
8. They also reduce free cytosolic Ca+2 by
9. Preventing release from a. Sarcoplasmic reticulum
b. Increase Ca+2 efflux
By this way it causes vasodilation/ relaxation.
• Other effects:
1. Dilation of skin blood vessels= flushing/ shining
effects
2. Headache
3. Relax Bronchioles
In case of emergency we administer them via
sub lingual route.
 Calcium channel blockers
• Blocks the channels for the entry of Ca+2

• Ca+2 channels are responsible for the influx of

Ca+2 ions
• By the entry of Ca+2 from ECF to ICF causes
the contraction of muscles ( smooth muscles)
more specifically arterioles.
• In angina the balance between oxygen supply
and demand is disturbed.
• Ca channel blockers causes decrease in
peripheral vascular resistance.
• More oxygen will be supplied to the heart
walls.
• Voltage sensitive channel activated at -40mV
• Receptor operated channel activated by
binding of agonist.
• Leak channel activated by mechanical stress.
• Voltage sensitive: L-type channel blocker
which is Nifedipine and verapamil.
• Ca channel blockers binds to open or
inactivate state of channels.
• Ca channel blockers bind with L-type of receptor
and prevents entry of Ca+2 into the cell.
• Causes arterioles dilation and decrease PVR.
• Ca entry into the cell causes increase synthesis of
Ca from sarcoplasm reticulum and contractility is
increased.
• Decrease myocardial contraction and causes HR
to decrease and also force of contraction to
decrease.
• It will decrease the myocardial work load, so
simply we reduced the oxygen demand.
Β-blockers and K+ channel opener
• In angina the demand of O2 and supply of O2
is disturbed.
• Β-blockers decrease the activation of heart by
blocking Β1
• They decrease work of heart by decreasing
HR, contractility and BP.
• Β-blockers are drug of choice for effort
induced angina.
• They are in active against vasospsatic angina
• All B blocker are non selective at high doses.
• In classical angina= B-blockers+Nitrate
• They are contraindicated in asthma, diabetes
and bradycardia.