Physiology - Renin Angiotensin system Flashcards by Jenna Dymond

which of these is not a major compound of the RAAS?

a.angiotensin 1
b. angiotensin 2
c. aldosterone
d,renin

a.angiotensin 1

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what triggers the RAAS?

a. dehydration, sodium deficiency, haemorrhage
b. hypertension
c. low blood pressure
d. dehydration, sodium increase

a.dehydration, sodium deficiency, haemorrhage

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what happens following sodium defficiency and dehydration?

a. increased renin
b. increased ahngiotensin 1
c. decrease in blood volume and pressure
d. increase in blood volume and pressure

c. decrease in blood volume and pressure

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where is renin secreted?

a. proximal convuluted tubule
b. juxtaglomerular cells of afferent arterioles in kidneys
c. juxtaglomerular cells of efferent arterioles in kidneys
d. glomerulus
e. macula densa

b. juxtaglomerular cells of afferent arterioles in kidneys

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what is the primary determinant of RAAS activity?

a. rate of angiotensin 1 conversion
b. sodium levels
c. renin secretion rate

c.renin secretion rate

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what does hypovolaemia refer to?

a. low extracellular fluid
b. high extracellular flid
c. low intracellular fluid
d. high intracellular potassium

a.low extracellular fluid

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what detects the low perfusion pressure of the kidney caused by dehydration etc?

a. baroreceptors
b. glomerulus
c. macula densa cells
d. juxtaglomerular cells of afferent arteriole

a.baroreceptors

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what type of cells detect decreased plasma sodium in the DCT/ reduced glomerular filtration in order to trigger renin secretion?

a. baroreceptors
b. glomerulus
c. macula densa cells
d. juxtaglomerular cells of afferent arteriole

c. macula densa cells

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which of these does not cause increased renin secretion?

a. sympathetic stimulation of the juxtaglomerular apparatus
b. decreased sodium in the distal convuluted tubules
c. decreased perfusion pressure
d. decreased potassium in plasma

d.decreased potassium in plasma

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what causes sympathetic stimulation of the juxtaglomerular apparatus?

a. stress/trauma
b. inflammation
c. arousal
d. infection

a.stress/trauma

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which receptor is activated by stress/ trauma ?

a. a1 adrenergic receptor
b. a1 cholinergic receptor
c. b1 adrenergic receptor
d. b2 adrenergic receptor

c. b1 adrenergic receptor

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Hypovolaemia
B. Low blood pressure
C. Low plasma electrolyte levels
D. Low glomerular filtrate 
electrolyte levels
E. Noradrenaline

d. low glomerular filtrate electrolyte levels

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where is angiotensinogen released from?

a. juxtaglomerular cells of the kidneys
b. liver
c. lungs
d. macula densa

b.liver

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what is the role of angiotensin converting enzyme?

a. converts angiotensin to agt 1
b. converts agt 2 to agt 1
c. converts agt 1 to agt
d. converts agt 1 to agt 2

d. converts agt 1 to agt 2

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where is ACE found?

a. juxtaglomerular cells of the kidneys
b. liver
c. lungs
d. macula densa

c.lungs

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where is aldosterone secreted from in response to increased agt 2?

a. juxtaglomerular cells of the kidneys
b. liver
c. lungs
d. adrenal cortex

d.adrenal cortex

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what is released from the adrenal cortex?

a. agt 1
b. aldosterone
c. agt
d. agt 2
e. renin

b.aldosterone

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what is the effect of increased aldosterone release from the adrenal cortex?

a. increased sodium and water reabsorption , increased potassium and H+ excretion in urine at kidneys
b. decreased sodium and water reabsorption , increased potassium and H+ excretion in urine at kidneys
b. decreased sodium and water reabsorption , decreased potassium and H+ excretion in urine at kidneys

a.increased sodium and water reabsorption , increased potassium and H+ excretion in urine at kidneys

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which statement is true of agt 2 ?

a. it is a weak vasoconstrictor
b. it is a weak vasodilator
c. it is a strong vasodilator
d. it is a potent vasoconstrictor

d.it is a potent vasoconstrictor

raises peripheral resistance and BP

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which substance promotes ADH (vasopression) release which expands extracellular volume and vasoconstricts?

a. agt
b. agt 1
c. agt 2
d. aldosterone

d.agt 2

agt 2 faciliates the release of which substance by postganglionic sympathetic neurons?

a. adrenaline
b. norepinephrine
c. epinephrine
d. noradrenaline

b.norepinephrine

agt increases Na and H2O reabsorption from where?

a. DCT
b. kidneys
c. PCT
d. glomerulus

c.PCT

Which is an indirect function of angiotensin II?
A. Increases water reabsorption in 
nephron
B. Inhibits thirst
C. Releases aldosterone from 
pituitary gland
D. Releases ADH from adrenal 
gland
E. Relaxes vascular smooth 
muscle

A. Increases water reabsorption in

nephron

where is ADH released from?

a. adrenal cortex
b. pituitary gland
c. kidneys
b. liver
d. lungs

b.pituitary gland

what are the two types of agt 2 receptor? a. Agt 1 and Agt2 b. a1 and a2 c. b1 and b2 d. AT1 and AT2

d.AT1 and AT2

which agt 2 receptor is found on vascular smooth muscle cells, the brain, kidney and adrenal cortex? a. AT1 b. AT2

a.AT1

which agt 2 receptor is found in the fetus and brain of adults with expression falling after birth? a. AT1 b. AT2

b.AT2

which agt 2 receptor mediates most of the effects of agt 2? a. AT1 b. AT2

a.AT1

what type of receptor are the AT receptors? a. g protein linked b. muscarinic d. nicotinic

a.g protein linked

what is the g protein of an AT1 receptor linked to in vascular smooth muscle? a. PL-1 b. PL-D c. PL-2 d. PL-C

d.PL-C

what does agt do in smooth muscle? a. increase ca2+ so contracts b. decreases ca2+ so contracts c. increases ca2+ so relaxes d. decreases ca2+ so relaxes

a.increase ca2+ so contracts

activation of which agt receptor leads to activation of tyrosine kinases? a. AT1 b. AT2

a.AT1

what is the G protein of AT2 receptors linked to? a. PL-C b. tyrosine kinases c. phosphatases

c. phosphatases

what do phosphatases do when activatd by AT2 receptor activation by agt2? a. agonise growth effects, close K+ channels, decrease NO production b. antagonise growth effects, open K+ channels, increase NO production

b.antagonise growth effects, open K+ channels, increase NO production

what effect does AT2 activation have on K+ channels? a. opens b. closes

a.opens

a tumour secreting which substance can lead to hypertension through RAAS overactivity? a. aldosterone b. renin c. agt 2 d. agt 1

b.renin

how does renal artery stenosis lead to hypertension?

constriction of renal artery by atherosclerotic plaque reduced perfusion pressure renin secretion blood pressure increase

which of these does not lead to hypertension due to RAAS overactivity? a. renin secreting tumour b. increased agt 2 production c. increased angiotensinogen production d. renal artery stenosis

b. increased agt 2 production

what type of drug is propanolol? a. B adrenergic blocker b. renin inhibitor c. prostaglandin synthesis inhibitor d. ACE inhibitor

a.B adrenergic blocker

which of these drugs is a b adrenergic blocker? a. propanolol b. indomethacin c. pepstatin and enalkiren d. catopril and enalapril e. losartan

a.propanolol

which of these drugs is an inhibitor of prostaglandin synthesis? a. propanolol b. indomethacin c. pepstatin and enalkiren d. catopril and enalapril e. losartan

b.indomethacin

which of these drugs is a renin inhibitor? a. propanolol b. indomethacin c. pepstatin and enalkiren d. catopril and enalapril e. losartan

c.pepstatin and enalkiren

which of these drugs is a ACE inhibitor ? a. propanolol b. indomethacin c. pepstatin and enalkiren d. catopril and enalapril e. losartan

d.catopril and enalapril

which of these drugs is an AT receptor antagonist / blocker ? a. propanolol b. indomethacin c. pepstatin and enalkiren d. catopril and enalapril e. losartan

e.losartan

what type of drug is indomethacin? a. B adrenergic blocker b. renin inhibitor c. prostaglandin synthesis inhibitor d. ACE inhibitor

c.prostaglandin synthesis inhibitor

what type of drug is pepstaton and enalkiren ? a. B adrenergic blocker b. renin inhibitor c. prostaglandin synthesis inhibitor d. ACE inhibitor

b.renin inhibitor

what type of drug is catopril and enalapril ? a. B adrenergic blocker b. renin inhibitor c. prostaglandin synthesis inhibitor d. ACE inhibitor

d.ACE inhibitor

what type of drug is losartan? a. B adrenergic blocker b. renin inhibitor c. prostaglandin synthesis inhibitor d. ACE inhibitor e. AT receptor antagonists/blockers

e. AT receptor antagonists/blockers

How do ACE inhibitors lower blood pressure? A. Increase the degradation of bradykinin B. Inhibit angiotensin converting enzyme, which disrupts the production of angiotensin 1 from angiotensin 2 C. Inhibit renin, which disrupts the production of angiotensin 1 from angiotensinogen D. Inhibit renin, which disrupts the production of angiotensin 2 from angiotensinogen E. Inhibit angiotensin converting enzyme, which disrupts the production angiotensin 2 from angiotensin 1

E. Inhibit angiotensin converting enzyme, which disrupts the production angiotensin 2 from angiotensin 1