Renal Blood Flow

Question 1

What are the three types of nephron?

Answer 1

Superficial
Cortical
Juxtomedullary

Question 2

Describe superficial nephrons

Answer 2

Glomerulus is very close to the surface
Very short LoH
Blood supply from interlobular artery

Question 3

Describe cortical nephrons

Answer 3

Glomerulus in the middle of the cortex

LoH goes just into the medulla

Question 4

Describe juxtomedullary nephrons

Answer 4

7% of nephrons
Glomerulus very close to cortical-medullary border
Very long LoH

Question 5

Describe the blood supply for superficial and mid cortical nephrons

Answer 5

Renal blood supply enters from left/right renal artery -> Branches to segmental, interlobal, arcuate and interlobular arteries
Each nephron receives one afferent arteriole
Divides into a capillary network with a glomerulus
Reunites to form efferent tubule
Divides to form the peritubular plexus surrounding the capillaries
Then have peritubular venule, interlobar vein and renal vein exits kidney

Question 6

Describe the blood supply for juxtamedullary nephrons

Answer 6

left/right renal artery enters -> branches into segmental, interlobar, arcuate and interlobular arteries. Each nephrons receives one afferent arteriole.
This divides into a capillary network with the glomerulus, and reunite to form efferent arteriole.
This efferent arteriole penetrates deep into medulla as VASA RECTA vessels
Then divides to form the peritubular capillaries surrounding medullary segments of nephrons.
Peritubular venule, interlobal vein and renal vein exits kidney

Question 7

Describe the magnitude and distribution of renal blood flow within the kidney

Answer 7

The kidneys receive around 340ml/min (25% of CO)

Cortex receives ~93%, Medulla receives ~7% and papilla receives ~1% of renal blood flow

Question 8

How does the difference in the renal blood flow between cortex and medulla relate to their function?

Answer 8

Cortex = site of all glomeruli - function is to filter all the blood. Also has PCTs where the majority of reabsorption of solutes and water occurs. Also site where waste products and drug molecules are added to filtrate. All this requires a high blood supply

Medulla = site of responsible for making a concentrated urine - generation of a hyperosmotic interstitium, and a low blood flow ensures it isnt washed out. Medullary blood supply arranged in loop to generate counter current exchange of solutes

Question 9

Describe the main sites of vascular resistance within the renal circulation

Answer 9

Renal circulation has afferent and efferent arterioles for resistance (afferent- glomerulus- efferent)
These two sites maintain the filtration pressure across the length of the capillary bed, whereas the pressure would drop off along a systemic capillary

Question 10

How is the RBF and GFR be altered by the afferent and efferent arterioles?

Answer 10

Afferent = Constriction causes decreased in RBF, FP and GFR. Dilation causes increased RBF, FP and GFR

Efferent = Constriction decreases RBF but increases FP and GFR. Dilation causes increased RBF but decreases FP and GFR

Question 11

How can RBF be measured?

Answer 11

Clearance of PAH, or contrast enhanced ultrasound in a clinical setting

Question 12

What is the main mediator of keeping RBF and GFR constant?

Answer 12

Afferent resistance - without a mechanism, the RBF and GFR would fluctuate wildly due to changes in systemic BP and BF.

if RBF is kept constant, then GFR is kept constant

Question 13

What are the two mechanisms of autoregulation?

Answer 13

Myogenic reflex and Tubular-Glomerular feedback

Question 14

Describe the myogenic reflex of autoregulation

Answer 14

Stretch of a blood vessel caused by increased blood flow results in a reflex contraction of the VSM, increasing the resistance to flow.
- increased flow activates stretch activated Ca channels, bringing in calcium and causing contraction. This decreases the RBF and so protects the glomerulus from large changes in FP

Question 15

Describe the Tubular glomerular feedback mechanism of autoregulation

Answer 15

When there is an increase in BP, GFR and FP will increase. This means that there will be an increase in delivery of NaCl to the DCT. Macula densa cells (part of juxtoglomerular apparatus) sense this, as they will be transporting more NaCl. This transport is energy expensive, and so more adenosine is produced, This adenosine acts as a local hormone, diffuses to the afferent arteriole where it acts on A1 receptors, causing Ca entry and smooth muscle contraction. This increases the resistance and so stabilises the RBF and GFR

Question 16

What local hormone and neuronal responses are there to blood loss?

Answer 16

Maintenance of the systemic BP is the main priority, and this can affect the RBF and GFR.

Na is released from the renal sympathetic nerve, adrenaline is released from the adrenal gland and AngII is generated after a rise in plasma renin

Question 17

How does the efferent arteriole try to stabilise the GFR and RBF after blood loss and local hormone action?

Answer 17

The efferent arteriole is sensitive to AngII mediate vasoconstriction. It is also more sensitive than the afferent to both adrenaline and NA. Therefore, in a moderate blood loss, they primarily act upon the efferent arteriole, causing vasoconstriction. This causes a drop in RBF, but increases GFR. This means that although blood is partitioned away from the kidney, the impact on GFR is minimised

Question 18

How does the afferent arteriole try to stabilise the GFR and RBF after blood loss and local hormone action?

Answer 18

AngII has no effect on the afferent arteriole. However, at higher concentrations, both adrenaline and NA act on the afferent arteriole to cause vasoconstriction. This gives a substantial drop in RBF and GFR, as blood is diverted to systemic circulation to bolster BP. This ‘shut down’ of RBF may result in acute or chronic kidney damage

Question 19

How is the kidney protected from anoxic damage during haemorrhage?

Answer 19

Anoxia in the kidney causes a release of PGs. These act on the afferent arteriole to generate vasodilation. The small reduction in vessel town causes a small but significant increase in RBF, which can protect the kidney (particularly medulla) from ischaemic damage.

Question 20

Why may NSAIDs been dangerous in patients with renal problems?

Answer 20

Prostaglandin synthesis is inhibited by NSAIDs.
A patient with compromised renal haemodynamics may have an increased risk of renal failure, and so should not take NSAIDs.