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Flashcards in RAAS Deck (18):
1

What does RAAS stand for?

Renin-Angiotensin-Aldosterone System

2

How does it control blood pressure?

1. By controlling/altering vascular tone (smooth muscle relaxation or contraction on the blood vessels) (Angiotensin II)

2. By controlling natriuresis (The amount of Na+ excreted in the urine) which will therefore effect the blood volume. (Aldosterone)

3

What does RAAS activation cause?

An increase in vascular tone and an increase in blood volume (less Na+ excreted) and therefore higher blood pressure.

4

What is Renin and where is it produced?

Renin is a proteolytic enzyme produced by the juxtaglomerular cells of the Kidney that is responsible for converting angiotensinogen to angiotensin I and this is subsequently then converted to angiotensin II by ACE (angiotensin converting enzyme).

5

What does it mean by the RAAS works synergistically with the SNS?

Both SNS activation/stimulation and RAAS activation result in increased BP. SNS also acts as a stimulator for RAAS activation.

6

Where is ACE found?

Released from endothelial cells all around the body but primarily located in the lungs.

7

What is the action of angiotensin II?

It is a potent vasoconstrictor - it binds to smooth muscle of blood vessels causing contraction and therefore increasing blood pressure.

8

What is the drug target of Angiotensin II and what is its mechanism of action?

It binds to AT-1 receptors and these are a type of G coupled protein receptor. The activation of the G protein alpha subunit activated phospholipase C which then triggers the cleavage of IP3 from PIP3 and this results in increased intracellular calcium. Increased intracellular calcium leads to muscle contraction hence vasoconstriction.

9

Angiotensin II can be further cleaved into Angiotensin III and IV, what are the actions of these two proteins?

Angiotensin III = stimulates production of Aldosterone
Angiotensin IV = inhibition of clot clearance

10

What factors might promote the release of aldosterone?

A variety of factors including high K+ levels and AT-1 activation (binding of Angiotensin II or III)

11

Where is the receptor target of Aldosterone?

In the collecting tubules of the Kidneys (one of the last passages the urine travels through)

12

What is the effect of aldosterone binding to the receptors in the collecting tubule?

It results in the expression of more Na+ channels and Na/K transporters in the collecting tubule thus more Na+ is reabsorbed from the urine and so more fluid is retained.

13

What are the main two drugs targeting RAAS (targeting angiotensin II and aldosterone)

ACE inhibitors - block the enzyme ACE from converting Angiotensinogen I to II by competitively binding to the ACE catalytic site

ARB's (angiotensin receptors blockers) - block angiotensin II from binding to the AT-1 receptors in blood vessels

14

What are the some of the dual undesirable effects of ACE inhibitors?

They can restrict the breakdown of bradykinin which can result in a dry cough and angioedema. Angioedema is abnormal swelling and inflammation and is often in the lips, mouth, pharynx.

15

Not many people get the adverse effects of ACE inhibitors (as a result of increased bradykinin) but if they do, what should you do?

Cease the ACE inhibitor medication

16

Which is more effective, ACE I's, ARB's or both?

ACE I's.

Using both is dangeroud as it could cause an increased risk of hyperkalaemia or acute kidney injury.

17

Aldosterone antagonists are another class of drug targeting the RAAS, what does it mean by antagonist?

These drugs will bind to the aldosterone receptor but will not cause all cellular response - they will just prevent aldosterone from bindng.

18

Which drugs affecting RAAS act on; ezymes, receptors and ion channels

Enzymes = ACE inhibitors
Receptors = ARB's. beta blockers. aldosterone antagonists
Ion channels = diuretics, calcium channel blockers