Renin-Angiotensin System

Front 1

renin is produced where?

Back 1

granular cells of the afferent arterioles of the juxtaglomerular apparatus

Front 2

renin does what?

Back 2

converts angiotensinogen to angiotensin I

Front 3

what happens to angiotensin I and how is it done?

Back 3

it is converted to angiotensin II by ACE

Front 4

what is ACE and where is it produced?

Back 4

angiotensin converting enzyme (ACE) is produced in the capillaries of the lungs

Front 5

what does angiotensin II do?

Back 5

1) vasoconstrictor --> ↑blood pressure
2) stimulates aldosterone production by the suprarenal cortex

Front 6

where is angiotensinogen produced?

Back 6

liver

Front 7

in general, what does aldosterone do?

Back 7

↑ reabsorption of Na+ in renal tubule --> ↑ water accompanying
--> ↑blood volume and pressure

Front 8

what 3 mechanisms stimulate renin production?

Back 8

1) low renal perfusion pressure directly stimulates the granular cells to produce renin
2) sympathetic nerves stimulate secretion of renin from the granular cells
3) signals from the macula densa when renal tubular fluid is low cause granular cells to release renin

Front 9

what is the effect of aldosterone on K+

Back 9

↑ K+ secretion in the late distal tubule and collecting duct
--> ↓ K+ in blood
mechanism = ↑ luminal membrane K+ channels and stimulate the Na+-K+ pump
--> ↑K+ uptake into the principal cells
--> ↑the intracellular [K+] and the driving force for K+ secretion

Front 10

how do ACE inhibitors work and what is the result?

Back 10

ACE inhibitors (eg. captopril) block the conversion of angiotensin I to angiotensin II
--> ↓ blood pressure

Front 11

what are AT1 antagonists and what to they do?

Back 11

Angiotensin receptor antagonists (eg. lorsartan) block the action of antiogensin II at its receptor
--> ↓blood pressure

Front 12

list 4 specific mechanisms of angiotensin II

Back 12

1) stimulates synthesis & secretion of aldosterone by adrenal cortex
2) ↑Na+-H+ exchange in the proximal convoluted tubule --> ↑ Na+ reabsorption
3) ↑ thirst
4) vasoconstriction of the arterioles --> ↑ TPR and ↑ aterial pressure

Front 13

what is the RAAS and what kind of overall regulation does it do?

Back 13

renin-angiotensin-aldosterone system is used in long-term blood pressure regulation by adjustment of blood volume via slow, hormonal mechanisms

Front 14

decreased renal perfusion causes ??

Back 14

↑ renin --> ↑angiotensin I --> ↑ angiotensin II -->
1) ↑aldosterone --> ↑Na+ reabsorption
2) ↑ Na+-H+ exchange --> ↑ Na+ reabsorption
3) ↑ thirst
4) vasoconstriction --> ↑ TPR

Front 15

which are physiologically active of angiotensin I and II?

Back 15

angiotensin I is inactive
angiotensin II is active

Front 16

how is angiotensin II degraded and what is the result?

Back 16

angiotensin II is degraded by angiotensinase and one of the peptide fragments is angiotensin III which has some of the biological activity of angiotensin II

Front 17

how is aldosterone secretion controlled?

Back 17

under tonic control by ACTH and separately regulated by the renin-angiotensin system and by K+

Front 18

how does ACTH affect aldosterone?

Back 18

ACTH --> cholesterol desmolase cholesterol --> pregnenolone --> progesterone --> 11-deoxycorticosterone --> corticosterone --> aldosterone

Front 19

where in the path from ACTH to aldosterone does angiotensin II act

Back 19

last step of corticosteron --> aldosterone

Front 20

where does angiotensin II act?

Back 20

in the zona glomerulosa of the adrenal cortex
--> ↑ corticosteron --> aldosterone

Front 21

what are the 3 effects of aldosterone?

Back 21

1) ↑ renal Na+ reabsorption
2) ↑ K+ secretion
3) ↑ renal H+ secretion
1 & 2 principal cells of the late distal tubule and collecting duct
3 α-intercalated cells of the late distal tubule and collecting duct