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Antihypetensive Drugs
Antihypetensive Drugs
GUMS
The Heart
Introduction
Hypertension
Stroke Heart
Rate CRITICAL POINT!
Volume Change any physical factors
controlling CO and/or TPR and
MAP can be altered.
Contractility Filling Pressure
1. Neural 2. Hormonal
SymNS Renal
PSNS Ang II
Adrenal
Catecholamines
Aldosterone
CRITICAL POINTS!
1. These organ systems and mechanisms control physical factors of CO and
2. Therefore, they are the targets of antihypertensive therapy.
Types of
Hypertension
Essential Secondary
Environmental
Factors
Step 2
Diuretic with beta blocker
Sympatholytics
Step 3
Direct-acting vasodilator
Sympatholytic with diuretic
Step 4
Adrenergic neuron blocker
Combinations from steps I, II & III
Antihypertensive Drugs
◼ Diuretics:
◼ Thiazides: Hydrochlorothiazide, chlorthalidone
◼ High ceiling: Furosemide
◼ K+ sparing: Spironolactone, triamterene and amiloride
MOA: Acts on Kidneys to increase excretion of Na and H2O –
decrease in blood volume – decreased BP
◼ Angiotensin-converting Enzyme (ACE) inhibitors:
◼ Captopril, lisinopril., enalapril, ramipril and fosinopril
MOA: Inhibit synthesis of Angiotensin II – decrease in peripheral
resistance and blood volume
◼ Angiotensin (AT1) blockers:
◼ Losartan, candesartan, valsartan and telmisartan
MOA: Blocks binding of Angiotensin II to its receptors
Antihypertensive Drugs
◼ Centrally acting:
◼ Clonidine, methyldopa
Increased
Blood Vol.
Rise in BP
Vasoconstriction
Kidney
(Adrenal cortex)
RAS – actions of Angiotensin-II.
1. Powerful vasoconstrictor particularly arteriolar – direct action and
release of Adr/NA release
◼ Promotes movement of fluid from vascular to extravascular
◼ More potent vasopressor agent than NA – promotes Na+ and water
reabsorption
◼ It increases myocardial force of contraction (CA++ influx promotion)
and increases heart rate by sympathetic activity, but reflex
bradycardia occurs
◼ Cardiac output is reduced and cardiac work increases
2. Aldosterone secretion stimulation – retention of Na++ in body
3. Vasoconstriction of renal arterioles – rise in IGP – glomerular damage
4. Decreases NO release
5. Decreases Fibrinolysis in blood
6. Induces drinking behaviour and ADH release by acting in CNS –
increase thirst
7. Mitogenic effect – cell proliferation
Angiotensin-II
◼ What are the ill effects on chronic ?
◼ Volume overload and increased t.p.r
◼ Cardiac hypertrophy and remodeling
Myocardial Infarction
b-blockers
ACE inhibitors
Diabetes
ACE Inhibitors
AVOID- b-blockers
Renal Insufficiency
ACE Inhibitors
Angina
b-blocker
Calcium channel antagonists
Asthma
Ca++ channel blockers
AVOID- b-blockers