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renal > Volume regulation L11 > Flashcards

Volume regulation L11 Flashcards

1
Q

How can the body measure its effective circulating volume?

A

body can measure volume in different parts of circulation due to presence of pressure sensors and volume sensors that are mediated by stretch, found within the cardiovascular system

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2
Q

What effect does a haemorrhage have on circulating volume and total extracellular volume?

A
  • haemorrhage decreases circulating volume
  • this decreases pressure in circulation
  • fluid drawn from extracellular space into circulation down a pressure gradient
  • total extracellular volume falls too
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3
Q

What is the juxtaglomerular apparatus?

A

juxta- next to
glomerular - glomerulus
=structures next to the glomerulus

  • consists of renal afferent arteriole (granular cells) and distal convoluted tubule (macula densa)
  • regulates filtration rate and blood pressure across glomerulus
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4
Q

What are granular cells?

A
  • also known as juxtaglomerular cells
  • present mainly in renal afferent arteriole (although a few on efferent)
  • secrete renin
  • stimulated by macula densa cells (detect fall in Na+) or stretch receptors that detect drops in blood pressure
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5
Q

Describe the renin-angiotensin-aldosterone cycle

A
  • low Na+ in distal tubule
  • detected by macula dense cells
  • stimulate juxtaglomerular cells to produce renin
  • renin converts angiotensinogen (produced in liver) into angiotensin I
  • angiotensin I travels in circulation to lungs
  • angiontensin converting enzyme (ACE) (produced in lungs) converts angiotensin I into angiotensin II
  • angiotensin II stimulates the adrenal cortex to secrete aldosterone
  • aldosterone travels to the kidney where it increases Na+ reabsorption in distal tubule and collecting ducts
  • angiotensin II also increases Na+ reabsorption in proximal tubule (Na+/H+ exchanger) as well as efferent arteriole vasoconstriction
  • Na+ concentration increases
  • GFR increases
  • blood pressure increases due to H20 retention
  • negative feedback on system
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6
Q

what are the two main physiological triggers for aldosterone release?

A
  • stimulation through angiotensin II

- hyperkalaemia

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7
Q

List the four groups of drugs that can inhibit the renin angiotensin system. What is the ultimate goal of inhibiting this system?

A
  • ACE inhibitors
  • Angiotensin II receptor antagonists (same as AT1-receptor antagonists)
  • aldosterone receptor antagonists
  • drugs that inhibit renin

decrease blood pressure

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8
Q

Give examples of ACE inhibitors.

A

ramipril, captopril, enalopril *prils

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9
Q

Give examples of AT1 receptor antagonists.

A

candesartan, irbesartan, valsartan, losartan *sartans

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10
Q

Give examples of aldosterone receptor antagonists.

A

spironolactone *look back to previous lectures!

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11
Q

Give examples of renin inhibitors.

A

aliskiren

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12
Q

Describe the cellular pathway that AT1 exhibits to produce responses in circulation.

A
  • AT1 coupled to Gq protein
  • Gq stimulates Phospholipase C
  • PLC ultimately forms IP3 and DAG (and PiP2)
  • IP3 and DAG stimulate Ca2+ release from intracelullar stores
  • increased released of Ca2+ in smooth muscle cells can stimulate vasoconstriciton
  • Ca2+ release in granular can stimulate them to release more renin
  • both actions increase blood pressure
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13
Q

What is a side effect of taking ACE inhibitors?

A

cough

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14
Q

What are the five ways angiotensin II increases circulating volume?

A
  • vasoconstriction
  • stimulates aldosterone release from adrenal cortex > increase distal Na+ absorption
  • increase Na+/H+ exchange in proximal tubule, hence proximal Na+ and water absorption
  • cause ADH release
  • causes thirst
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15
Q

The sympathetic nervous system can cause renin to be released from granule cells in afferent arteriole. Describe the three mechanisms of action through which this happens.

A
  1. Direct stimulation of renin release from granule cells
  2. sympathetic nerves release noradrenaline > detected by alpha-1 adrenoceptors on vascular muscle cells in afferent arteriole > vasoconstriction upstream from granular cells > fall in pressure downstream > sensed by beta-1 adrenoceptors on granule cell (stretch-sensitive) > renin release
  3. vasoconstriction of afferent arteriole (same as above) > decrease in pressure downstream (to glomerulus) > drop in glomerular hydrostatic pressure > decrease in GFR > renin angiotensin system stimulation through Na+ concentration
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16
Q

What are the effects of beta-blockers in the kidney?

A
  • block beta-1 adrenoceptors in afferent arteriole
  • reduce renin production
  • lower blood pressure
17
Q

How can a fall in blood volume stimulate renin release from kidney?

A

-lower blood volume = fall in venous pressure
> decreased cardiac output
> decreased blood pressure
> fall in pressure in vasa recta
> increase in fluid uptake from interstitium
> greater loss of fluid from filtrate (gradient)
> decrease in Na+ delivery to distal tubule
> detected by macula densa
> renin release from granule cells

18
Q

How can a fall in blood volume stimulate ADH release from kidney?

A
  • decreased cardiac filling >activation of baroreceptor reflex
  • angiotensin II stimulates ADH release
  • ADH release > increase in water reabsorption > increase in cirulating volume (however this response does decrease osmolality as does not affect Na+ reabsorption)
19
Q

What body stimuli activate ADH release?

A
  • increased osmolaliy
  • stress
  • decreased volume
  • nicotine
20
Q

What body stimuli inhibit ADH release?

A
  • decreased osmolality
  • increased volume
  • alcohol
21
Q

What is ANP? What does it do?

A

-Atrial Natriuretic Peptide
-released due to increased atrial filling (due to increased venous return)
-travels to kidney and acts on ANPa,b recpetors
> increases cGMP activity (second messenger)

ANP has different actions that all ultimately increase renal Na+ excretion (natriuretic):

  • inhibits Na+/K+ ATPase > dilates afferent arteriole > increases GFR > increase Na+ to kidney > inhibits renin release
  • decreases Na/Cl cotransport activity in distal tubule
  • decreases ENaC activity in collecting duct
22
Q

Which prostaglandins are natriuretic?

A

PGE2 and PGI2

*can be inhibited by NSAIDS > Na+ retention

23
Q

Where is dopamine synthesised?

A

epithelial cells in proximal tubule of kidney

24
Q

How does dopamine increase Na+ excretion?

A

-acts on D1 receptors to increase cAMP
-also acts to decrease activity of Na+/H+ exchanger in proximal tubule
>increased Na+ excretion

renal (16 decks)

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