The Renin-Angiotensin-Aldosterone-System (RAAS)

Question 1

• How does ANP control blood volume?

Answer 1

Increased blood volume stretches arterial walls causing release of ANP from the atria, ANP decreases reabsorption of Na thus decreasing blood volume

Question 2

• Where is angiotensinogen release from? And what happens to it?

Answer 2

Liver, cleaved by renin to form angiotensin I

Question 3

• Where is ANGI I activated to ANG II by ACE?

Answer 3

Surface of endothelial cells in the pulmonary circulation

Question 4

• What are the main effects of ANG II?

Answer 4

Acts on specific AT1 receptors – causes vasoconstriction & stimulates the release of aldosterone from the ZG of the adrenal cortex

Question 5

• What is the difference between acute and chronic pressure natriuresis?

Answer 5

Acute is without other compensatory mechanisms

Question 6

• What other effects can ANG II have?

Answer 6

Insertion of Na+ channels in renal tubules via AT1

Question 7

• Where is renin synthesised?

Answer 7

Juxtaglomerular cells (kidneys)

Question 8

• What two factors increase renin output from the juxtaglomerular cells?

Answer 8

Decreased stretch & SNS activation

Question 9

• If intra-renal mechanisms are exhausted and plasma [Na+] are still not in balance what is required?

Answer 9

System wide reaction – blood pressure, hormonal and SNS changes

Question 10

• How does aldosterone affect Na+ and K+?

Answer 10

Increased resorption of Na+, increased secretion of K+