the renin angiotensin andosterone system

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The Renin Angiotensin Aldosterone System (RAAS) By: Darya Osman Hussein Daoud

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Page 1: The Renin Angiotensin Andosterone System

The Renin Angiotensin Aldosterone System (RAAS)By: Darya Osman Hussein Daoud

Page 2: The Renin Angiotensin Andosterone System

Content

What is the Rennin-Angiotensin-Aldosterone System?

Role it plays in Hypertension

Drugs affecting system

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What is it?

A hormone system Regulates blood pressure and fluid balance Involve kidney and Liver

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Important Factors

Renin Angiotensinogen Angiotensin I Angiotensin II Aldosterone

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Renin

A.K.A. Angiotensinogenase

Released from Kidney

Hydrolyzes angiotensinogen

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Angiotensinogen

Produced and released by liver Level increased by corticosteroids, estrogen and thyroid hormone Composed of 453 A.A. but the 1st 12 are the most important

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Angiotensin I Produced in the kidney through action of Renin on Angiotensinogen Has no biological activity Precursor to Angiotensin II

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Angiotensin II Produced by ACE in lungs Main hormone responsible for increase in blood pressure Stimulates Na reabsorption and H+ secretion in proximal tubules of kidney

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Angiotensin III

Has 40%activity of angiotensin II Has aldosterone producing activity Causes increase in mean arterial pressure

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ACE

Angiotensin Converting Enzyme Acts in the lungs Catalyzes conversion of Angiotensin I to

Angiotensin II Degrades bradykinin and other vasoactive

peptides

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Types of drugs

I. Angiotensin Converting Enzyme inhibitors (ACE inhibitors)

II. Renin inhibitors

III. Angiotensin II Receptor Blockers (ARBs)

IV. Aldosterone receptor antagonists

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I. ACE Inhibitors (Captopril, Enalapril,Lisinopril)

Used as 1st line treatment for hypertension in patients with: High risk of CAD Diabetes History of stroke Heart failure MI Chronic kidney disease

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I. ACE Inhibitors

Action: Reduce peripheral vascular resistance No increase in CO,HR or contractility Cause vasodilation of arterioles and veins Decrease aldosterone secretion Reduce cardiac work by decreasing pre and afterload

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I. ACE Inhibitors

Pharmacokinetics: Orally bioavailable Given as drug or prodrug Captopril and Lisinopril do not require hepatic activation (used in hepatic

impairment) Fosinopril not eliminated by kidney (used in renal impairment) Enalaprilat only one given via IV

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I. ACE Inhibitors

Clinical Use: Hypertension Heart failure Ventricular dysfunction following MI Diabetic nephropathy

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I. ACE Inhibitors

Adverse effects: Hypotension Dry cough Angioedema Renal failure Skin rash Hyperkalemia Altered taste Teratogenic

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I. ACE Inhibitors Advantage

Protect kidneys from kidney damage/failure in diabetics

Prevent micro-albuminuria

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II. Renin Inhibitors

Selective inhibitor – Aliskiren

Action: Lowers BP Usually used as monotherapy

Side effects: Causes diarrhea at high doses Contraindicated in pregnancy Causes cough and angioedema

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III. ARBs (Losartan, Valsartan, Candesartan) Action:

Lower BP by decreasing vasoconstrictor tone

Mechanism of Action: Block action of angiotensin II on angiotensin II receptor

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III. ARBs

Pharmacokinetics Given orally T ½ = 1 – 2 hours

Clinical Use Hypertension CHF nephropathy

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III. ARBs

Adverse Effects Hypotension Dizziness Hyperkalemia (rare)

Special points No dry cough No angioedema