Renal Blood Flow And Gfr Flashcards
Describe renal blood flow
• Input
– Renal artery
• Renal Blood Flow (RBF) is ~1.1L/min
• All blood flows through the glomeruli in the cortex
What is Renal plasma flow and how is it calculated
• What is the Renal Plasma Flow (RPF)?
Difference between RBF and RPF is haematocrit
Normally proportion of 45% is red blood cells and the rest is plasma. Plasma is what going to be filtered
– Haematocrit (Ht or HCT or erythrocyte volume fraction (EVF) is the
volume percentage (%) of red blood cells in blood)
• Normally ~0.45,
• RBF is 1.1L /min
• We can now calculate RPF
– 0.55 x 1.1L /min = 605 mL/min of plasma
What is a renal lobe and the associated blood vessels
5 segmental arteries
Lobe is pyramid + cortex immediately above it. Edged by blood vessels
Running between lobes is an arter and vein. Interlobar arteies and veins. Drain into renal vein. Forming an arch over the pyramids . Accurate artery and vein. Front h e. Accurate vessels, penetrating into the cortex - end vessels - these are the interlobular vessels - within the lobe.
Glomeruli arise from interlobular vessels in the cortex.
The afferent arteriolar longs interlobular artery with glomerulus. Leaves through the efferent arteriola
Describe.2 types of nephron
Capillary bed followe by capillary bed. Both able to venoconstrict. 2 subtypes related to 2 types of nephrons
Majority to of nephrons - peritubular capillaries - these are a random arrangement of capillary bed - no order or structure. 85-90% of nephrons
Second type of nephron that is not - juxtamedualry nephrons - nephrons where the glomerulus ‘tis close to the boundary between cortex and medulla - glomerulus sits much lower down in cortex. Also the peritubular capillary organisation is very specific. Majority of LOH is in medulla . The specialist organisation of capillaries is the vasa recta. Vessels run parallel with LOH
Compare cortical and juxtamedulalry nephrons
See slide
What is not filtered though the glomerulus
RBS, WBCs and albumin not filtered. Remaining is almost identical to plasma
Describe the glomerulus as a filter
• Found only in the cortex • 20% of blood from renal artery is filtered at any one time
• The normal total glomerular filtrate
per day is 140 – 180 L /day (~125
ml/min)
• 80% blood arriving exits via efferent arteriole (unfiltered) - RBCs WBCs and albumin stay in renal plasma. The 80% that si not filtered carries the extra from the 20% that was filtered.
• Always the same despite two types of kidney nephrons
• Cortical
• Juxtamedullary
Compare plasma and ultra filtrate
See slide
Describe the histology of a renal corpuscle
See slide. Filtrate leaves capillaries and goes int Bowman s space. Drains into PCT. PCT has mitochondria, microvilli. DCT has bugger lumen, no invagination or microvilli.
What are the 3 layers of filtration
If glom gets blocked it cant filter. Or it can get holes in it. Which will let stuff through that it shouldnt..
Endothelium - gaps in the endothelium. Leaky. Basement membrane is acellular and gelatinous. Forms part of the filtration process. On the outside of basement membrain there are pod oocytes. Pedicels sit on basement membrane. Gap between pedicels = filtration slit.
How is the basement membrane specialised to block small proteins
Basement membrane is charged. It has glycoproteins in it. Glycoproteins carry negative charge. This means that when other proteins that might be small enough to get through endothelium fenestrations, the negative charge of glycoproteins on basement membrane repels them away . That is a way to prevent small proteins getting into the filtrate
Describe the perm selectivity. In terms of size
Size of slits limit what will get through.
Small mol.Wt. and effective radius less than 1.48 nm will pass through
Small proteins repelled by -ve charge
Describe selectivity in terms of charge
Positive charge and small size - can get through easily. With a positive charge, if a bit bigger can still get though.
With a negative charge, even if they are small enough, negative charge will prevent
In many disease processes the negative charge on the filtration barrier is lost so that proteins are more readily filtered - a condition called proteinuria
What is net filtration pressure
Fluid arriving into space - PGC. Get filtration bc of this pressure.
Fluid in bowman capsule has hydrostatic pressure too. PBC. This pushes back against PGC. Theres is also opposition by oncotic pressure. The oncotic pressure is being excepted by oncotic proteins WITHIN the glomerulus. Draws water towards glomerulus. Oncotic force on water
Hydrostatic pressure in the capillary –. regulated (PGC)
+ Hydrostatic pressure in the Bowman’s capsule (PBC)
+ Oncotic pressure difference between
the capillary and tubular lumen (πGC)
= net filtration pressure
What are teh forces tat determine net filtration pressure
A (PGC) hydrostatic pressure in plasma Favours filtration 50mmHg
B (PBC ) hydrostatic pressure in tubule Opposes filtration 15mmHg
C (πGC) Oncotic pressure in glomerulus Opposes filtration 25mmHg
Harder to leave thru efferent art bc diameter is smaller. This causes filtration to happen.
Oncotic pressure gets higher towards the end of glomerulus .. high aconcotic force remains in efferent arteriole.
Describe aytoregulation
Harder to leave thru efferent art bc diameter is smaller. This causes filtration to happen.
Oncotic pressure gets higher towards the end of glomerulus .. high aconcotic force remains in efferent arteriole.
• Autoregulation is able to maintain GFR when blood pressure is within physiological limits (80-180 mmHg). Changes tone depending on blood pressure.
• Auto-regulatory mechanisms keep GFR within normal limits
• ↑ blood pressure → afferent
arteriole constriction
• ↓ blood pressure → afferent arteriole dilatation
If pressure on AA declines, AA will relax. If less blood trying to flow through, less pressure, AA walls relax., more blood is able to get into glomerulus.
= GFR is unchanged
How is PGC regulated
• Arterial smooth muscle responds to increases and decreases in vascular wall tension • It contributes to total auto- regulatory mechanism • Occurs rapidly (3-10 s ) • It is a property predominantly of the preglomerular resistance vessels – accurate, – interlobular – Afferent arteriole
What can be done myogenically to control GFR
Both AA and EE are capable of constricted or dilated.
to decrease GFR could constrict AA. Or could dilate EA but if we date EA, give blood free pass without filtration bc takes path of least resistance - not good in unhealthy kidney
If wanted to cause increase in GFR, can constrict A even more, increase hydrostatic pressure, increase GFR. OR could maximally dilate AA, letting more blood in therefore increasing GFR
What is tubuloglomerular feedback
• This mechanism links sodium and chloride concentration at the
macula densa with control of renal arteriolar resistance
• Its acts in response to acute perturbations in the delivery of fluid and solutes to the JGA.
• It has 2 components
Afferent arteriole resistance
Efferent arteriolar feedback ( hormonal)
• Controls the distal solute delivery and hence tubular reabsorption
What is the function of the macula dense cells
Within distal tubule - macula dense cells. Sense these changes.
Changes of flow rate in distal tubule aresensed by macula senda cells. If increase in art pressure that means increase in GFR, more sodium and more chloride - greater filtered load.. GFR an Luminl NaCl are proportional. Linear relationship . That means there is linear elation ship between GFR and renal plasma flow. Autoreulation tried to blunt this, but there is a linear relationship and kidney is trying to keep it low
Give a summary of the chain of events of the TGF response
Vasoconstriction reduce the GFR which reduces NaCl bc vasoconstriction/ but still will be a change Macula sensation detect this change. They do this though NKCC2 channel. Increased conc of NaCl in macula dense - triggers release of ATP. Increase of NaCl also inhibits renin release in juctaaglomerular granular cells.
ATp levels in macula dense cells then increase. As ATP reaves macula dense through exit channels. It’s quickly converted to AMP and ends up as adenosine..Adenosine binds to A1 receptors. These are coated on cells that surround AA. G protein coupled response. Gi causes inhibition of adenylate cyclase. G0 signalling leads to increase in IC conc of calcium. If IC calcium increases, that spreads through gap junctions into smooth muscle cells. This causes even more constriction of AA. This additional vasoconstriction=toon rly important in regulating
This is feedback from DCT to AA
Give an overview f what happens if NaCl increases or decreases
• If NaCl increases
– response is GFR needs to decrease
– adenosine released mainly causes vasocontraction of the AE via A1
receptors but vasodilation of EA by A2 receptors is also found
– Reduces pressure gradient across glomerulus and thus slows GFR
• If NaCl decreases
– response is GFR needs to increase
– prostaglandins released causes vasodilatation of AA
Adenosine and prostaglandin relationship - affect tone of AA
• The relationship between GFR and distal salt concentration only applies in acute changes
• long-standing primary disturbance in body fluid volume are not regulated like this more later…
Describe neural regulation on GFR
Sympathetic nerve fibres innervate AE and EA • Normally sympathetic innervation is low ( no effect of GFR)
• Fight or Flight Or ischaemia Or haemorrhage (sever) can stimulate renal vessels
• Vasoconstriction occurs as a result which conserves blood volume (haemorrhage) and can cause a fall in GFR
(NB) Parasympathetic NS (ACh) release of NO for endothelial
cells and vasodilation
Give an overview of glomerulartubular balance
Job of PCT.
amount of reabsorption in PCT changes bc of around of filtered old. Itsis limiting the amount of damage that is going to be caused by increase or decrease in GFR.
Autoregulation of GFR prevents GFR from changing too much
• 1st line of defence Myogenic and TG
feedback
• 2nd line of defence
• Glomerulotubular Balance blunts
sodium excretion response to any
GFR changes which do occur despite 1st line responses
