Antihypertensive drugs, classification & their MOA with suitable examples class lecture ppt

1. Antihypertensive Drugs
Assist. Professor
Department of Pharmacy
SRU, Raipur, (C.G.)

2. Antihypertensive Drugs
Hypertension: Hypertension is a very common
disorder, particularly past middle age. It is not
a disease in itself, but is an important risk
factor for cardiovascular mortality and
morbidity.
Antihypertensive Drugs: These are drugs used
to lower BP in hypertension.

3. CLASSIFICATION
1. Diuretics:
• Thiazides: Hydrochlorothiazide,
• Chlorthalidone, Indapamide
• High ceiling: Furosemide, etc.
• K+ Sparing: Spironolactone, Amiloride
2. ACE inhibitors:
• Captopril, Enalapril, Lisinopril,
• Perindopril, Ramipril, Fosinopril, etc.
3. Angiotensin (AT1 receptor) blockers:
• Losartan, Candesartan, Irbesartan, Valsartan,
• Telmisartan
4. Direct renin inhibitor:
• Aliskiren
5. Calcium channel blockers:
• Verapamil, Diltiazem, Nifedipine, Felodipine,
• Amlodipine, Nitrendipine, Lacidipine, etc.

4. CLASSIFICATION
6. β Adrenergic blockers:
• Propranolol, Metoprolol, Atenolol, etc.
7. β + α Adrenergic blockers:
• Labetalol, Carvedilol
8. α Adrenergic blockers:
• Prazosin, Terazosin, Doxazosin
• Phentolamine, Phenoxybenzamine
9. Central sympatholytics:
• Clonidine, Methyldopa
10. Vasodilators:
• Arteriolar: Hydralazine, Minoxidil,
• Diazoxide
• Arteriolar + venous: Sodium nitroprusside

5. Mechanism of action
1. Diuretics:
a. Thiazide:
Thiazide block the Na+Cl- Symporter in distal tubule
Leading to fall the cardiac output
Result fall in BP

6. b. High Ceiling Diuretic:
High ceiling diuretic action on the Na+K+2Cl- inhibite in AScLH
Reduction of the plasma volume and decrease the cardiac output
Decrease BP
c. K+ Sparing Diuretic:
K+ sparing diuretic lower the BP slightly but they are use in
conjugation with thiazide
Augument the antihypertensive action

7. 2. ACE Inhibitors:
ACE inhibitors are first choice drugs for hpertension
ACE inhibitors are inhibit the conversion of A-I to A-II
for the therapy of hypertension
A-II induced vasoconstriction and raises BP & A-II
increase force of myocardial contraction by promoting
Ca++ influx
ACE inhibitor are block the conversion of A-I to A-II
Lower BP

8. 3. Angiotensin blockers(AT1):
AT1 blocker are block the AT1 angiotensin-II receptor
Resulting the relaxation of smooth muscles & promote
vassodilation
Increase renal salt & water excreation
Also reduce plasma volume & decrease cellular
hypertrophy

9. 4. Calcium Channel Blockers:
Calcium channel blocker having +ve inotropic effect
bromotropic action
All ca++ channel blocker lower BP by inhibiting Ca++
influx of Ca++ channel
Leading to smooth muscle relaxation & decrease vascular
peripheral resistance
Result fall in BP

10. 5. Beta-adrenergic Blockers:
Beta-blockers basically in heart decrease heart
rate & decrease force of contraction
Decrease cardiac output & the result decreases
peripheral resistance on each blood vessel
Decrease BP

11. 6.Alpha+Beta-adrenergic blockers:
It is a combined alpha 7 beta blockers reduce t.p.r.
Reduce the pressure & usefull in the treatment of
hypertension
7. Alpha-adrenergic blockers:
It is prototype alpha1 antagonist dilate both
resistance & capitance vessels
Reduction in t.p.r. & BP with only slight decrease in
venous return and cardiac output are similar to
that produced by a direct acting vassodilator

12. 8. Central Sympatholytics: Methyl-Dopa
It is alpha-methyl analogue of dopa, the precursor of
dopamine DA & NA
The alpha methyl-NA (Alpha2-agonist) form in the
brain and act alpha-2 receptor to decrease efferent
sympathetic activity
Methyl dopa decrease (t.p.r. ) total peripheral resistance
more than H.R. or C.O.
Fall in B.P.

13. 9. Vasodilators : Nitrates
Organic nitrates are rapidly denitrated enzymatically in the
smooth muscle cell to release the reactive free radical nitric
oxide (NO) which activates cytosolic guanylyl
Increased cGMP
causes dephosphorylation of myosin light chain kinase
(MLCK) through a cGMP dependent protein kinase .
Reduced availability of phosphorylated (active) MLCK
interferes with activation of myosin
it fails to interact with actin to cause contraction.
Consequently relaxation occurs. Raised intracellular cGMP
may also reduce Ca2+ entry
contributing to relaxation.

14. Pharmacokinetic: Captoprill
Absorption: 70% orally administration
Distribution: BBB poor penetration
Metabolism: Metabolized by liver
Excretion: Unchanged in urine
Use:
• Hypertension
• C.H.F.
• Myocardial Infarction
• Diabetic nephropathy

15. Adverse effect:
 Hypotension
Cough
Rashes
Angioedema

16. References
• Tripathi KD, “Essentials of Medical
Pharmacology” published by Jaypee Brothers
Medical Publishers (P) Ltd, Seventh Edition:
2013, New Delhi, p.p. no-558-570.