Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
21 Cards in this Set
- Front
- Back
renin is produced where?
|
granular cells of the afferent arterioles of the juxtaglomerular apparatus
|
|
renin does what?
|
converts angiotensinogen to angiotensin I
|
|
what happens to angiotensin I and how is it done?
|
it is converted to angiotensin II by ACE
|
|
what is ACE and where is it produced?
|
angiotensin converting enzyme (ACE) is produced in the capillaries of the lungs
|
|
what does angiotensin II do?
|
1) vasoconstrictor --> ↑blood pressure
2) stimulates aldosterone production by the suprarenal cortex |
|
where is angiotensinogen produced?
|
liver
|
|
in general, what does aldosterone do?
|
↑ reabsorption of Na+ in renal tubule --> ↑ water accompanying
--> ↑blood volume and pressure |
|
what 3 mechanisms stimulate renin production?
|
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 |
|
what is the effect of aldosterone on K+
|
↑ 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 |
|
how do ACE inhibitors work and what is the result?
|
ACE inhibitors (eg. captopril) block the conversion of angiotensin I to angiotensin II
--> ↓ blood pressure |
|
what are AT1 antagonists and what to they do?
|
Angiotensin receptor antagonists (eg. lorsartan) block the action of antiogensin II at its receptor
--> ↓blood pressure |
|
list 4 specific mechanisms of angiotensin II
|
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 |
|
what is the RAAS and what kind of overall regulation does it do?
|
renin-angiotensin-aldosterone system is used in long-term blood pressure regulation by adjustment of blood volume via slow, hormonal mechanisms
|
|
decreased renal perfusion causes ??
|
↑ renin --> ↑angiotensin I --> ↑ angiotensin II -->
1) ↑aldosterone --> ↑Na+ reabsorption 2) ↑ Na+-H+ exchange --> ↑ Na+ reabsorption 3) ↑ thirst 4) vasoconstriction --> ↑ TPR |
|
which are physiologically active of angiotensin I and II?
|
angiotensin I is inactive
angiotensin II is active |
|
how is angiotensin II degraded and what is the result?
|
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
|
|
how is aldosterone secretion controlled?
|
under tonic control by ACTH and separately regulated by the renin-angiotensin system and by K+
|
|
how does ACTH affect aldosterone?
|
ACTH --> cholesterol desmolase cholesterol --> pregnenolone --> progesterone --> 11-deoxycorticosterone --> corticosterone --> aldosterone
|
|
where in the path from ACTH to aldosterone does angiotensin II act
|
last step of corticosteron --> aldosterone
|
|
where does angiotensin II act?
|
in the zona glomerulosa of the adrenal cortex
--> ↑ corticosteron --> aldosterone |
|
what are the 3 effects of aldosterone?
|
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 |