Glomerular Filtration Rate

Glomerular Filtration Rate
Contents
1 Introduction
2 Regulation of the GFR
3 Regulation of Renal Blood Flow and Capillary Hydrostatic Pressure

3.1 Constriction of the Afferent and Efferent Arterioles
4 Physiological Regulators of GFR

o
4.1 Autoregulation
4.2 Angiotensin 2
4.3 Sympathetic Nervous System
4.4 Nitrous Oxide and Prostaglandins
4.4.1 Nitrous Oxide
4.4.2 Prostaglandins
4.4.3 Effects of Blocking Nitric Oxide or Prostaglandins
Introduction
The glomerular filtration rate or GFR is the amount of fluid filtered from the capillaries into the
Bowmans capsule of the kidneys per unit time. The GFR can be expressed as the following formula:
GFR = Kf x net filtration pressure

Kf = the filtration coefficent
Kf can furthermore be expressed by the following formula
Kf = membrane permeability x filtration area

The GFR is practically proportional to metabolic body mass. Therefore the bigger the animal the
greater the GFR.
Regulation of the GFR

The following formula helps us to understand GFR and how various factors affect it. Whilst
reading this article you may find it useful to refer back to it:
Q = (PA - PE) R
Q = Flow, PA = Pressure in afferent arteriole, PE = Pressure in efferent arteriole, R = Resistance
There are two major forces opposing GFR. These are the hydrostatic pressure in the Bowmans
space and the plasma protein osmotic pressure. These are not under physiological control. The
filtration coefficient is also beyond the realms of physiological control. On the other hand the
hydrostatic pressure in the capillaries and the renal blood flow are under physiological regulation and
adjust filtration according to the bodies needs.
Regulation of Renal Blood Flow and Capillary Hydrostatic

Pressure
These two factors are determined by the arterial blood pressure coupled with the contraction of both
the afferent and efferent arterioles. The total resistance of the afferent and efferent arterioles, which
is determined by the contraction of them, determines the renal blood flow and any particular arterial
pressure. Therefore it is important that they change with arterial pressure in order to maintain a
steady renal blood flow.
Constriction of the Afferent and Efferent Arterioles

Normally the afferent arteriole is of larger diameter than the efferent. This means there is high
resistance as the blood is forced from a wider vessel to a narrower one and this promotes filtration. If
the arterial blood pressure remains constant then contracting either vessel reduces blood flow as it
increases resistance. However contracting either has opposite effects on the filtration pressure. If
you contract the afferent arteriole there will be less of a pressure difference between the afferent and
efferent arteriole so there will be reduced filtration pressure. However if you constrict the efferent
arteriole you are increasing the pressure difference between the two and filtration pressure increase.
Overall the constriction of the afferent arteriole decreases both blood flow and filtration pressure
where as constricting the efferent arteriole decreases blood flow but increases filtration pressure.
(Both of these statements are assuming a constant blood pressure). The fact that both can be
altered allows independent regulation of both GFR and blood flow.
Physiological Regulators of GFR

The main systems which regulate renal blood flow and GFR are:
Autoregulation
Q = (PA - PE) R
Q = Flow, PA = Pressure in afferant arteriole, PE = Pressure in efferant arteriole, R = Resistance
If renal resistance to blood flow was constant then any change to mean arterial blood pressure
would alter blood flow, glomerular hydrostatic pressure and therefore filtration. However if blood
pressure is changed by a small amount over a short period of time blood flow and filtration to the
kidneys is not really affected. This is due to autoregulatory feedback mechanisms which allow the
kidney to vary the resistance in the afferent arteriole. If it wasn't for these autoregulatory
mechanisms then a small increase in arterial blood pressure would drastically increase the excretion
of salt and water leading to a drastic reduction in the concentration of NaCl in the ECF.
Pressure Autoregulation
If arterial blood pressure increases then resistance in the afferent arteriole increases also and the
opposite occurs if blood pressure falls. The role of pressure autoregulation is to ensure that during
transient changes in blood pressure there is little effect on renal blood flow and therefore filtration
providing the bodies need for the excretion of water and solutes remains the same. This is essential
as only a small change in renal blood flow and thus filtration rate can have a massive change on
urine output. The mechanisms for this response are found within the kidneys:
Myogenic Response
Stretching of blood vessels due to increased blood pressure results in the blood vessel
decreasing it's diameter.
This results in an increased resistance to blood flow
Thus keeping the GFR constant
Tubuloglomerular Feedback (TGF)
When blood pressure increases for a short amount of time more blood flows through the
glomerulus and therefore more filtrate is produced.
This results in a decrease in proximal tubule reabsorption
This increases the concentration of NaCl in the distal tubule which is detected by the Macula
Densa
This structure releases local factors resulting in the vasoconstriction of the afferent arteriole
If blood pressure decreases the opposite occurs
The Limitations of Autoregulation

Despite the efforts of the autoregulatory system an increase in blood pressure still leads to an
increased secretion of salt and water. This is because even a small percentage change in GFR
leads to large percentage change in the excretion of salt and water. This excretion is however far
less drastic than would be the case without autoregulation and actually helps to restore pressure to
normal. This increase in urinary output as a result of an increase in arterial blood pressure is
termed pressure diuresis.
Angiotensin 2
Sympathetic Nervous System
When the animal is in a situation of crisis or stress blood flow to the kidneys is reduced for the sake
of other organs such as the brain, heart and skeletal muscles. The sympathetic nervous system and
a heightened level of adrenalin in the plasma cause the contraction of both the afferant and efferant
arterioles. As the efferant arteriole is contracted alongside the afferant one there is still a pressure
differance allowing for filtration to still occur and reducing the impact on filtration compared to the
impact on blood flow. At times when sympathetic tone is very high the renal blood flow could be
reduced to 10-30% of normal. This practically stops filtration occuring and thus stops urine
production.
Resting Sympathetic Activity
Unlike many other organs the kidneys have a low resting sympathetic tone. Therefore the
sympathetic nervous system cannot effectively decrease the resistance by decreasing itself. This
suggests that its main aim is to compensate for a fall in blood pressure or to prepare the body for the
fight or flight response.
Effect on Reabsorption
As GFR is less affected than blood flow the filtration of what blood does pass through the glomerulus
is more efficent. This means that the blood entering the pertitubular capillaries will have a higher
protein osmotic pressure and a lower hydrostatic pressure as more of the plasma will have been
filtered. This causes greater reabsorption of water and salt from the tubules. This causes urine
volume to fall. It also stimulates renin, The Renin Angiotensin Aldosterone System
(RAAS) and aldosterone which all in turn have their effect on reabsorption.
Net Effect of Increased Sympathetic Nervous Activity on the Kidneys
Reduced renal blood flow
Small decrease in excreted waste
Increased conservation of water and sodium
Nitrous Oxide and Prostaglandins

Nitrous Oxide and Prostaglandins have an impact on arteriolar resistance. Their role in the regulation
of renal blood flow and filtration is however uncertain.
Nitrous Oxide
Mediates dilation in the cortical circulation
Prostaglandins
Mediates dilation in medullary circulation (cortical in extremes)
PGE2 is involved in the regulation of the reabsorption of sodium
Prostacyclin increases the secretion of potasium by stimulating renin secretion thus

activating the Renin-Angiotensin-Aldosterone System and as a result increasing the amount
of Aldosterone secreted.
Prostacyclin increases renal blood flow and gfr when circulating volume is
decreased. This results in increased tubular flow and increased potasium secretion
In healthy/hydrated individuals these compounds do not play a significant role in
sodium/water homeostasis
Effects of Blocking Nitric Oxide or Prostaglandins
Loss of medullary circulation - reduced ability to concentrate water
Loss of medullary flow - reduces the ability to preserve sodium balance and maintain normal
blood pressure
Loss of either may result in ischaemic damage

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Glomerular Filtration Rate

2 Regulation of the GFR

3 Regulation of Renal Blood Flow and Capillary Hydrostatic Pressure

4 Physiological Regulators of GFR

4.3 Sympathetic Nervous System

4.4 Nitrous Oxide and Prostaglandins

4.4.1 Nitrous Oxide

4.4.3 Effects of Blocking Nitric Oxide or Prostaglandins

GFR = Kf x net filtration pressure

Kf = membrane permeability x filtration area

Regulation of the GFR

Regulation of Renal Blood Flow and Capillary Hydrostatic

Constriction of the Afferent and Efferent Arterioles

Physiological Regulators of GFR

This results in an increased resistance to blood flow

Thus keeping the GFR constant

Tubuloglomerular Feedback (TGF)

This results in a decrease in proximal tubule reabsorption

If blood pressure decreases the opposite occurs

The Limitations of Autoregulation

Reduced renal blood flow

Small decrease in excreted waste

Increased conservation of water and sodium

Nitrous Oxide and Prostaglandins

Mediates dilation in the cortical circulation

Mediates dilation in medullary circulation (cortical in extremes)

PGE2 is involved in the regulation of the reabsorption of sodium

Prostacyclin increases the secretion of potasium by stimulating renin secretion thus

In healthy/hydrated individuals these compounds do not play a significant role in

Loss of medullary circulation - reduced ability to concentrate water

Loss of either may result in ischaemic damage

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