Test 2: lecture 24 RAAS

Question 1

steps of RAAS

Answer 1

angiotensinogen (renin) → angiotensin I (ACE) → angiotensin II

Question 2

ACE is a nonspecific enzyme that cleaves — from diverse substrates like —

Answer 2

dipeptides

bradykinin, angiotensin 1

Question 3

angiotensin III is formed by — and will cause — release

Answer 3

angiotensin II (ACE)

aldosterone release

Question 4

how does angiotensin degraded

Answer 4

angioteninases

enzyme breaks angiotensin down in 15-60 seconds

Question 5

aldosterone will —

Answer 5

cause Na and water retention

Question 6

what does angiotensin do

Answer 6

will cause vasoconstriction→ increases BP

causes aldosterone secretion → retension of water and Na from urine

Question 7

what triggers aldosterone release

Answer 7

increased angiotensin II, ACTH, low Na, high K
acidosis
atrial stretch receptors in response to low BP

aldosterone causes retention of Na and water, made by the zona glomerulosa of the adrenal gland

Question 8

aldosterone is made by —

Answer 8

zona glomerulosa cells in the adrenal cortex

Question 9

effects of RAAS on cardiovascular system

Answer 9

vasoconstriction

increased cardiac contractility with little change in heart rate

cause HTN/ fix low BP

Question 10

effect of RAAS on ANS

Answer 10

SYM: causes release of NE and enhances sensitivity of target tissues to NE

Adrenal medulla: causes release of catecholamines from chromaffin cells (↑ epi)

Question 11

RAAS effect on CNS

Answer 11

increase SYM
cause pituitary to release ADH and ACTH
cause increased thirst and need for salty things

Question 12

effect of RAAS on cell growth

Answer 12

cause cardiovascular hypertrophy

Question 13

overall effect of RAAS on the body

Answer 13

Question 14

AT1 receptors mediate —

Answer 14

most of the known functions of angiotensin

will cause smooth muscle contractions in seconds

GPCR receptor

Question 15

losartan works on what type of receptor

Answer 15

angiotensin 1 (AT1) receptor

Question 16

two major ways to block RAAS

Answer 16

ACE inhibitors

angiotensin II receptor blockers (ARBs)

Question 17

benefits of ACE inhibitiors

Answer 17

stops formation of angiotensin II

• decrease systemic vascular resistance without increasing heart rate
• promote natriuresis (pee out Na)
• treatment of hypertension, decrease mortality and morbidity in heart failure and left ventricular dysfunction after myocardial infarction
• delay diabetic nephropathy

Question 18

what are some side effects of ACE-inhibitors

Answer 18

will inhibit degradation of other substances (bradykinin and substance P)
cough
angioedema

ACE not specific for only angiotensin

Question 19

captopril

Answer 19

ACE inhibitor

will ↓BP and treat CHF

Question 20

what are some ACE inhibitors

Answer 20

enalapril, captopril, lisinopril

ACE-I= -pril

Question 21

losartan

Answer 21

nonpeptide antagonist of angiotensin 1 (AT1) receptor

does not effect AT2

used to treat HTN

Question 22

what are some ARBs

Answer 22

angiotensin receptor blockers/antagonists

peptide congeners: work in theory

nonpeptide antagonist: losartan, Azilsartan (Edarbi), Candesartan (Atacand), Eprosartan

ARBs — sartan

Question 23

angiotensin vs bradykinin

Answer 23

angiotensin: works to raise blood pressure

bradykinin acts to lower blood pressure (vasodilation)

Question 24

how to form kinins

Answer 24

kiniogens (kinogenases/kallikreins) →kinins

tissue damage and infections activate this class of compounds.

kallikrein-kinin system =KKS

Question 25

where do kallikreins come from

Answer 25

made in liver as prekallikreins cleaved to active **kallikrein** kallikrein will bind to kininogens to form kinins

Question 26

where to find kininogens

Answer 26

plasma, lymph , intersititial fluid in plasma: there are a high and low molecular weight versions **high**: stays in bloodstream **low**: can cross capillary walls into tissues

Question 27

what is the major form of kinins in plasma

Answer 27

bradykinin

Question 28

kininase II is the same as

Answer 28

ACE both work on many peptides: kinins and angiotensin

Question 29

which kinin receptor works on bradykinin and kallidin and what does it cause

Answer 29

B2 receptor a BGCR will cause vasodilation and excretion of Na and pain

Question 30

B2 kinin receptors will bind to --- and cause ---

Answer 30

bradykinin and kallidin Vasodilation, Na+ excretion, pain

Question 31

B1 kinin receptors binds to --- and cause ---

Answer 31

des-Arg kinins **(NOT bradykinin)** Vasoconstriction, pain, leukocyte recruitment

Question 32

what type of receptor has opposite effect as angiotensin 1 receptors

Answer 32

bradykinin B2 receptors B2 cause vasodilation and Na excretion AT1 cause vasoconstriction and Na retention

Question 33

why are ACE inhibitors cardioprotective

Answer 33

ACE inhibitors will **block angiotensin II** formation and will also **prevent the breakdown of bradykinin** ACE inhibitors will decrease BP and work to treat CHF (by getting rid of Na)