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Renal and Endocrine Biology > REB 24. Renin Angiotensin System > Flashcards

REB 24. Renin Angiotensin System Flashcards

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1
Q

What is the main driving pressure between the Intracellular Fluid (ICF) and Interstitial Fluid (IF)?

A

Osmotic Pressure

- e.g. ionic gradients

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2
Q

What is the main driving pressure between the Interstitial Fluid (IF) and Plasma?

A

Hydrostatic Pressure

- comes from the fluid inside the vessel pushing onwards

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3
Q

What compartment comprises of the largest total body water distribution percentage?

A

ICF comprises of 2/3 of TBW

ECF comprises of 1/3 TBW

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4
Q

What are the volumes of ECF and ICF present in the body?

A

65% ICF = 28L

35% ECF = 14L

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5
Q

What is the principle function of the renin-angiotensin system?

A

it controls fluid volume and blood pressure

- homeostasis

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6
Q

What happens to an individual in low blood pressure?

A

In low blood pressure, the oxygen perfusion is reduced
- causes lack of concentration, dizziness, nausea, fainting etc

then the RAAS responds!

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7
Q

Explain the RAAS system (the biochemical pathways) and processes involved.

A

[1] angiotensinogen synthesized in liver

[2] angiotensinogen converted to angiotensin I through the renin enzyme (endopeptidase)

*side note: renin is produced in the kidney

[3] angiotensin I is converted to angiotensin II through the ACE (angiotensin converting enzyme)

*side note: ACE is located in endothelial cells

[4a] angiotensin II converted to angiotensin III and angiotensin IV through the amino peptidase

[4b] angiotensin II activates to angiotensin II receptors which leads to a response

Response:

  • tubular reabsorption
  • aldosterone secretion
  • vasoconstriction
  • ADH release

— this increases the blood pressure!

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8
Q

Where is renin synthesized?

A

in the juxtaglomerular cells of the kidneys

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9
Q

Explain the process of the synthesis of renin. (e.g. what are the intermediates)

A 
[1] Preprorenin (406 AAs)
[2] Prorenin (383 AAs)
[3] Renin (340 AAs)
- stored in secretory granules
- released in response to low BP
- half life = 80 minutes 
- primary function is to cleave angiotensinogen to release angiotensin I
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10
Q

Where is renin stored?

A

in secretory granules

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11
Q

What is renin released in response to?

A

low BP

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12
Q

What is the half life of renin?

A

half life = 80 minutes

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13
Q

What is the rate-limiting step in the renin-angiotensin pathway?

A

renin

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14
Q

The activity of the renin-angiotensin system is measured clinically as?

A

PRA = Plasma Renin Activity

- used in diagnosis of patients with hypertension of hypotension

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15
Q

What is the juxtaglomerular apparatus made up of?

A

[1] Distal Convoluted Tubule

[2] Glomerular Afferent Arteriole

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16
Q

What are juxtaglomerular cells?

A
  • they are specialized smooth muscle cells in afferent arterioles on entry to glomeruli
  • they are site of renin synthesis
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17
Q

What is the Macula Densa?

A
  • modified epithelial cells of the DCT close proximity to juxtaglomerular cells
  • it senses NaCl uptake
  • when they sense decreased NaCl uptake they stimulate prostaglandins and releases renin
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18
Q

What are the factors that stimulate renin secretion?

A

[1] Decreased BP in the Afferent Arteriole
- sensed by baroreceptors in the juxtaglomerular cells

[2] Decreased NaCl Reabsorption

  • by Macula Densa Cells
  • MD cells stimulate release of renin from JG cells via prostaglandins

[3] Increased Adrenergic Activity

  • via sympathetic renal nerves + circulatory catecholamines
  • induce renin release via beta-adrenoreceptors
  • induce afferent arteriole constriction via alpha-adrenoreceptors
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19
Q

What are the factors that inhibit renin secretion?

A

[1] increasesd NaCl absorption across macula densa
[2] increased afferent arteriole pressure
[3] decreased sympathetic activity
[4] angiotensin II - negative feedback inhibition

20
Q

What are some CONDITIONS that increase renin secretion?

A

[1] Low Blood Pressure

  • sodium depletion
  • diuretics
  • haemorrhage
  • dehydration
  • heart failure
  • cirrhosis of liver

[2] Fight or Flight

  • sympathetic nervous system (increases circulating catecholamines)
  • plasma adrenaline (circulating adrenaline)
21
Q

What is a renin inhibitor that can be used to treat illness?

A

Aliskirin

- it is used to treat high blood pressure

22
Q

Describe the synthesis and processes involved in creating Angiotensin II

A

[1] Angiotensinogen

  • glycoprotein synthesized in LIVER
  • renin cleaves Leu-Val bond of angiotensinogen to form Angiotensin I

[2] Angiotensin I
- physiologically inactive

[3] ACE converts Angiotensin I into Angiotensin II

  • ACE primarily located in endothelial cells in LUNG
  • a carboxypeptidase enzyme removes His + Leu from carboxy terminus of angiotensin I
23
Q

Angiotensin II is the main what of RAAS?

A

main effector

24
Q

What are ACE inhibitors important for?

A

important drugs for reducing blood pressure (e.g. captopril)

25
Q

What are the 2 types of Angiotensin II receptors? Describe the function of each.

A

[1] AT1R (primarily mediates cardiovascular effects of ANGII)

  • AT1A = principally in blood vessels
  • AT1B = in adrenal cortex + anterior pituitary

[2] AT2R

  • more plentiful in foetus and neonate (functions are unclear)
  • activated by angiotensin III
26
Q

What are the biological actions of Angiotensin II, specifically with the AT1R receptor?

A

[1] tubular Na+ reabsorption
[2] vasoconstriction
[3] aldosterone release
[4] ADH release

[5] inhibits renin release from JG cells

27
Q

Explain how Angiotensin II stimulates sodium reabsorption

A
  • stimulates sodium reabsorption in renal tubules, particularly in the PCT
  • occurs via activation of AT1 receptors
  • – stimulates the Na+/K+ ATPase pump on the basolateral membrane
  • – stimulate NHE across the luminal membrane
  • – stimulates Na+/HCO3- co-transport across the basolateral membrane

NET EFFECT: ANG II-induced increases in Na+ absorption driving water absorption

28
Q

Explain how Angiotensin II stimulates vasoconstriction

A
  • increases overall systemic BP
  • in kidney, constriction of arterioles reduce filtration rate + urine production
  • reduced pressure in peritubular capillaries increases reabsorption

In other words…
- decreased pressure leads to increase in resorption

29
Q

Explain how Angiotensin II stimulates synthesis of aldosterone

A
  • stimulates aldosterone in zona glomerulosa of adrenal cortex
  • the zona glomerulosa of the adrenal gland…
  • — lacks 17-alpha hydroxylase activity
  • — has “aldosterone synthase” activity
30
Q

What are some characteristics of aldosterone?

A
  • mineralocorticoid
  • half life of about 20 mins
  • plasma levels vey low (0.17nmol/L) compared to cortisol (375nmol/L)
  • weakly bound to plasma protein
  • metabolised principally by liver
  • principal function (enhanced reabsorption of Na+ from distal convoluted tubules of kidney)
31
Q

What is hyperaldosteronism? What are the symptoms?

A

Hyperaldosteronism: too much aldosterone produced by adrenal glands

Symptoms:

  • hypertension
  • give/take hypokalaemia
32
Q

What are the 2 types of hyperaldosteronism?

A

[1] Primary Hyperaldosteronism

[2] Secondary Hyperaldosteronism

33
Q

What are the traits of Primary Hyperaldosteronism?

A
  • defect in ADRENAL GLANDS
  • increased levels caused by: adrenal adenoma (Conn’s syndrome) or idiopathic adrenal hyperplasia
  • diagnosed by decreased serum + increased aldosterone (renin-aldosterone ratio drops)
34
Q

What are the traits of Secondary Hyperaldosteronism?

A
  • decreased renal perfusion caused by:
  • — heart failure - decreased cardiac output
  • — nephrotic syndrome
  • — cirrhosis of liver
  • — renal artery constriction (stenosis)
35
Q

What is the diagnosis of primary hyperaldosteronism?

A
  • decreased renin

- increased aldosterone

36
Q

What is the treatment of hyperaldosteronism?

A 
aldosterone antagonist
(e.g. spironolactone)
37
Q

What is hypoaldosteronism?

A

too little aldosterone produced by adrenal glands

38
Q

What are the 2 types of hypoaldosteronism?

A

[1] Primary Hypoaldosteronism

[2] Secondary Hypoaldosteronism

39
Q

What are the traits of Primary Hypoaldosteronism?

A
  • occurs due to defective aldosterone release from the adrenals (e.g. Addison’s Disease)
  • autoimmune destruction of adrenal gland
  • — hypovolaemia with urinary Na+ loss and hyperkalemia
  • — postural hypotension
  • — dehydration
  • — adrenal crises due to severe adrenal insufficiency (due to damage to adrenal gland)
40
Q

What is the diagnosis of secondary hyperaldosteronism?

A
  • increased renin

- increased aldosterone

41
Q

What is the diagnosis of primary hypoaldosteronism?

A
  • decreased aldosterone

- increased renin

42
Q

What is the diagnosis of secondary hypoaldosteronism?

A
  • decreased aldosterone

- decreased renin

43
Q

What is the treatment of hypoaldosteronism?

A

mineralocorticoids

e.g. hydrocortisone, fludrocortisone + a high salt diet

44
Q

Explain how angiotensin II stimulates the antidiuretic hormone secretion

A
  • ADH is a peptide hormone produced in the pituitary gland
  • acts at AVP receptors (GPCRs)
  • half life of about 20 minutes
  • primary functions:
  • — vasoconstriction (mediated by AVP1R - Ca2+ release)
  • — increase water absorption in in the kidney (AVP2R - mediated by AVP2R - cAMP production)
45
Q

What is the function of antidiuretic hormone and how does it work?

A

ADH increases water absorption in collecting ducts
- due to increased luminal expression of Aquaporin 2

side note: ADH also promotes expression of urea transporters (UT-A) in the collecting duct

  • – facilitates absorption of urea into the medullary interstitium
  • – regulates fluid movement to and from collecting ducts

Renal and Endocrine Biology (25 decks)

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