Tubular glomerular feedback and kidney function Flashcards
1
Q
Which pressure differences allow filtration at the Bowman’s capsule?
A
- Hydrostatic pressure in the capillary
- Hydrostatic pressure in the Bowman’s capsule
- Oncotic pressure difference between capillary and Bowman’s capsule
2
Q
Outline the movement of water as it passes through the glomerulus
A
- Blood enters glomerulus at a really high pressure, which pushes lots of fluid into Bowman’s capsule
- Bowman’s capsule is full of fluid so starts pushing fluid back into capillaries
- Towards the end of the glomerulus, osmolality of blood has increased - water is drawn back into glomerulus from Bowman’s capsule
3
Q
What keeps renal blood flow and GFR fairly constant?
A
- Autoregulation by 2 mechanisms:
1. Myogenic mechanism
2. Tubuloglomerular feedback
4
Q
Why is it important that hydrostatic pressure within the glomerulus remains relatively constant?
A
- So it doesn’t damage the capillaries of the glomerulus irreversibly
5
Q
What is acute tubular necrosis?
A
- Occurs if BP in glomerulus drops too low
- Drop in blood flow through glomerulus causes blood flow through peritubular capillaries and Vasa recta to drop too
- Cells are damaged and die because they don’t receive oxygen or nutrients (can also occur due to toxic insult)
- Dead cells slough off and obstruct tubules of nephron
6
Q
What is the myogenic mechanism for regulating BP in the glomerulus
A
- Arterial smooth muscle responds to changes in vascular wall tension
- Occurs within 3-10s
- Property predominantly of preglomerular resistance vessels
- Accurate
- Main vessel involved is afferent arteriole
7
Q
Outline how the myogenic mechanism works
A
- If BP increases, afferent arteriole constricts and efferent arteriole dilates
- Causes decrease in GFR
- If BP decreases, afferent arteriole dilates and efferent arteriole constricts
- Causes increase in GFR
8
Q
What is tubuloglomerular feedback?
A
- Links Na+ and Cl- concentration at macula densa with control of renal arteriolar resistance
- Responds to acute disturbances in the delivery of fluid an solutes to JGA
- Controls distal solute delivery and tubular reabsorption
9
Q
What are the 2 components of tubuloglomerular feedback?
A
- Afferent arteriole resistance
- Efferent arteriolar feedback (hormonal)
10
Q
What is the response of tubuloglomerular feedback when BP is too high?
A
- When GFR and BP increase, concentration of Na+ and Cl- in cells increases
- Macula densa cells pump Na+ and Cl- out using the Na+/K+ ATPase
- When conc of Na+ and Cl- gets too high, ATPase can’t keep up
- Osmolality of macula densa cells therefore increases
- Water moves into cells, causing them to swell
- This stimulates the release of ATP and its conversion to adenosine
- Adenosine binds to A1 receptor on afferent arteriole
- Afferent arteriole constricts to reduce GFR
- Renin release is inhibited
11
Q
What is the response of tubuloglomerular feedback when BP is too low?
A
- Prostaglandins are released - cause vasodilation and increase BP
- Renin released by juxtaglomerular cells - activates RAAS
12
Q
What stimulates the release of renin?
A
- Increased sympathetic innervation
- Decreased wall tension of afferent arterioles
- Decreased Na+ to macula densa - stimulates release of prostaglandins, which then stimulate granular cells to secrete renin
13
Q
What is renin?
A
- A enzyme
- Synthesised and stored in the JGA in the kidneys
- A fall in plasma Na+ leads to a fall in extracellular fluid volume, stimulating renin release
14
Q
Outline RAAS
A
- Renin stimulates conversion of angiotensinogen to angiotensin I
- ACE stimulates conversion of angiotensin I to angiotensin II
- Angiotensin II stimulates release of aldosterone
15
Q
What are the effects of angiotensin II?
A
- Directly vasoconstricts efferent arterioles within glomerulus
- Releases ADH
- Stimulates thirst
- Stimulates release of aldosterone
