Cardio - CHF, RAAS

Question 1

In the short-term, RAAS is _____. Why?

Answer 1

great; BP is maintained in the face of low CO

Question 2

In the long-term, RAAS is _____. Why?

Answer 2

Terrible;

Cardiac fibrosis, renal damage, cytokine activation

Question 3

What are the RAAS activation events?

Answer 3

1. Juxtaglomerular apparatus releases renin
2. Renin converts angiotensinogen to angiotensin I
3. Angiotensin converting enzyme (ACE) converts ATI to ATII in the lungs

Question 4

What do the jusxtaglomerular cells detect?

Answer 4

Low BP, renal blood flow, or sodium

High SNS tone

Question 5

Where is angiotensinogen produced?

Answer 5

liver

Question 6

Where is ACE produced?

Answer 6

endothelial cells in the lungs

Question 7

What can you do if there is low BP?

Answer 7

Increase CO or VR (more volume or more vasoconstriction)

Question 8

What are the actions of ATII?

Answer 8

1. Increase volume
2. Increase vascular resistance
3. Negative effects on the heart

Question 9

Where does ATII act?

Answer 9

PCT to cause Na and water retention

Question 10

What does ATII stimulate?

Answer 10

Aldosterone release from the adrenals and ADH release from the posterior pituitary

Question 11

Where does aldosterone act?

Answer 11

DCT to retain Na and water (K loss)

Question 12

What does ADH do?

Answer 12

Inserts aquaporins into the DCT to allow for free water retention (without Na)

Question 13

What effect does ADH have on thirst?

Answer 13

Increases it by stimulating the thirst center in the hypothalamus

Question 14

What receptors does ATII bind and where?

Answer 14

AT receptors on the vessels leading to vasoconstriction

Question 15

ATII binds to the _____ arterial in the glomerulus, causing ____ and increasing intraglomerular pressure to maintin the _____.

Answer 15

efferent, vasconstriction, GFR

Question 16

What does ATII stimulate from the adrenal medulla?

Answer 16

Norepi release, which binds to alpha receptors on vessels causing vasoconstriction

Question 17

What does ATII stimulate that acts as a potent vasoconstrictor?

Answer 17

ADH release

Question 18

ATII –> excessive _____ retention –> _____ in a diseased heart

Answer 18

volume, CHF

Question 19

What are the negative effects of ATII and aldosterone on the heart?

Answer 19

They are cardiotoxic and cause fibrosis, vascular smooth muscle proliferation –> SHT, cytokines and free radical formation that lead to myocyte death

Question 20

ATII cause renal and arteriolar sclerosis leading to _____.

Answer 20

renal damage

Question 21

What are the 4 purposes of pharmacological intervention on RAAS?

Answer 21

1. Improve pumping function
   
   1. Better BP so RAAS isn’t stimulated
2. Stop or counteract RAAS activation/actions
3. Antihypertensive
   
   1. Counteracts vasoconstriction
4. Cardio-protective agents
   
   1. Reduce fibrosis, CK formation, increased cell death, vascular disease