This presentation briefly describes the pharmacology of cardiovascular system

1. Drugs Acting on Heart &Drugs Acting on Heart &
Cardiovascular SystemCardiovascular System
Drugs Acting on Heart &Drugs Acting on Heart &
Cardiovascular SystemCardiovascular System
Antihypertensive Agents-
•Calcium channel blocker
•Adrenergic agents
•Diuretics
•Vasodilators
•Angiotensin converting enzyme inhibitors
•Angiotensin II receptor blockers
 Drug of Cardiac Failure-
•Digoxin and Digitoxin -Cardiac Glycosides
•Bipyridine Derivatives -Milrinone and Inamrinone
Antihypertensive Agents-
•Calcium channel blocker
•Adrenergic agents
•Diuretics
•Vasodilators
•Angiotensin converting enzyme inhibitors
•Angiotensin II receptor blockers
 Drug of Cardiac Failure-
•Digoxin and Digitoxin -Cardiac Glycosides
•Bipyridine Derivatives -Milrinone and Inamrinone

2.  Anti-arrhythmic Drugs-
•Sodium channel blockers
•Beta Adrenergic Blockers
•Potassium channel blockers
•Calcium channel blockers
 Drug of Ischemic Heart Disease-
•Organic Nitrates
•Calcium Channel Blockers in Ischemic Heart Disease
•Potassium Channel Openers
 Anti-arrhythmic Drugs-
•Sodium channel blockers
•Beta Adrenergic Blockers
•Potassium channel blockers
•Calcium channel blockers
 Drug of Ischemic Heart Disease-
•Organic Nitrates
•Calcium Channel Blockers in Ischemic Heart Disease
•Potassium Channel Openers

3. Calcium Channel BlockersCalcium Channel BlockersCalcium Channel BlockersCalcium Channel Blockers
 Mechanism:
 blocking the binding of calcium to its receptors
 preventing muscle contraction
 decreased peripheral smooth muscle tone
 decreased systemic vascular resistance
 Resulting decreased blood pressure
 Mechanism:
 blocking the binding of calcium to its receptors
 preventing muscle contraction
 decreased peripheral smooth muscle tone
 decreased systemic vascular resistance
 Resulting decreased blood pressure

4. Diuretics & VasodilatorsDiuretics & VasodilatorsDiuretics & VasodilatorsDiuretics & Vasodilators
Mechanism of Diuretics-
 Decrease the plasma and
extracellular fluid volumes
 Resulting decreased preload
 decreased cardiac output,
 decreased total peripheral
resistance
 Overall effect: decreased
workload of the heart, and
decreased blood pressure
Mechanism of Diuretics-
 Decrease the plasma and
extracellular fluid volumes
 Resulting decreased preload
 decreased cardiac output,
 decreased total peripheral
resistance
 Overall effect: decreased
workload of the heart, and
decreased blood pressure
Mechanism of Vasodilators-
 Directly relaxes arteriolar
smooth muscle
 Resulting decreased systemic
vascular response
 decreased after load &
peripheral vasodilatation
Mechanism of Vasodilators-
 Directly relaxes arteriolar
smooth muscle
 Resulting decreased systemic
vascular response
 decreased after load &
peripheral vasodilatation

5. Cardiac GlycosideCardiac GlycosideCardiac GlycosideCardiac Glycoside
 Cardiac glycosides are naturally occurring plant substances that have
characteristic effects on the cardiac muscle. These specific compounds
contain a carbohydrate molecule.
 CHO molecule combined with water,
 converted into a simple sugar plus 1 or more active substances.
 Glycosides may actually work by blocking certain ionic pumps in the
cellular membrane.
 This action, indirectly increases the calcium concentration reaching the
contractile proteins.
 e.g digoxin (Lanoxin); it is used to treat heart failure and to treat certain
types of tachycardias.
 Cardiac glycosides are naturally occurring plant substances that have
characteristic effects on the cardiac muscle. These specific compounds
contain a carbohydrate molecule.
 CHO molecule combined with water,
 converted into a simple sugar plus 1 or more active substances.
 Glycosides may actually work by blocking certain ionic pumps in the
cellular membrane.
 This action, indirectly increases the calcium concentration reaching the
contractile proteins.
 e.g digoxin (Lanoxin); it is used to treat heart failure and to treat certain
types of tachycardias.

6. Alpha1 BlockersAlpha1 BlockersAlpha1 BlockersAlpha1 Blockers
Mechanism of Action
 Block the alpha1-adrenergic receptors
 SNS is not stimulated
 Resulting decreased blood pressure
Mechanism of Action
 Block the alpha1-adrenergic receptors
 SNS is not stimulated
 Resulting decreased blood pressure

7. Beta BlockerBeta BlockerBeta BlockerBeta Blocker
Block beta adrenergic receptors in the sympathetic nervous system
Very beneficial in people who have had myocardial infarctions,
especially those with low ejection fraction
Reduce workload of heart
Increase survival rates, decrease hospitalizations.
Block beta adrenergic receptors in the sympathetic nervous system
Very beneficial in people who have had myocardial infarctions,
especially those with low ejection fraction
Reduce workload of heart
Increase survival rates, decrease hospitalizations.

8. Angiotensin-converting Enzyme InhibitorsAngiotensin-converting Enzyme InhibitorsAngiotensin-converting Enzyme InhibitorsAngiotensin-converting Enzyme Inhibitors
 Large group of safe and effective drugs
 Often used as first-line agents for CHF and hypertension
 May be combined with a thiazide diuretic or calcium channel blocker
 Large group of safe and effective drugs
 Often used as first-line agents for CHF and hypertension
 May be combined with a thiazide diuretic or calcium channel blocker
Mechanism -RAAS: Renin Angiotensin-Aldosterone System
 When the enzyme angiotensin I is converted to angiotensin II, the
result is potent vasoconstriction and stimulation of aldosterone
 Result of vasoconstriction: increased systemic vascular resistance and
increased after load
 Therefore, increased BP
Mechanism -RAAS: Renin Angiotensin-Aldosterone System
 When the enzyme angiotensin I is converted to angiotensin II, the
result is potent vasoconstriction and stimulation of aldosterone
 Result of vasoconstriction: increased systemic vascular resistance and
increased after load
 Therefore, increased BP

9. Mechanism-ACE Inhibitors
Aldosterone stimulates water and sodium resorption.
Resulting increased blood volume
ACE Inhibitors block the angiotensin-converting enzyme, thus
preventing the formation of angiotensin II.
Also prevent the breakdown of the vasodilating substance, bradykinin
Resulting decreased systemic vascular resistance (afterload),
vasodilation and
therefore, decreased blood pressure
Mechanism-ACE Inhibitors
Aldosterone stimulates water and sodium resorption.
Resulting increased blood volume
ACE Inhibitors block the angiotensin-converting enzyme, thus
preventing the formation of angiotensin II.
Also prevent the breakdown of the vasodilating substance, bradykinin
Resulting decreased systemic vascular resistance (afterload),
vasodilation and
therefore, decreased blood pressure

10. Angiotensin II Receptor BlockersAngiotensin II Receptor Blockers Angiotensin II Receptor BlockersAngiotensin II Receptor Blockers
Mechanism of Action
Allow angiotensin I to be converted to angiotensin II, but
block the receptors that receive angiotensin II
Block vasoconstriction and release of aldosterone
Mechanism of Action
Allow angiotensin I to be converted to angiotensin II, but
block the receptors that receive angiotensin II
Block vasoconstriction and release of aldosterone