Difference between revisions of "Glomerular Filtration Rate"
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<center><big>'''Q = (PA - PE) ÷ R'''</big></center> | <center><big>'''Q = (PA - PE) ÷ R'''</big></center> | ||
+ | |||
'''Q''' = Flow, '''PA''' = Pressure in afferent arteriole, '''PE''' = Pressure in efferent arteriole, '''R''' = Resistance | '''Q''' = Flow, '''PA''' = Pressure in afferent arteriole, '''PE''' = Pressure in efferent arteriole, '''R''' = Resistance | ||
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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. | 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. | 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. | 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. | ||
Line 32: | Line 33: | ||
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. | 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: | The main systems which regulate renal blood flow and GFR are: | ||
− | ''' | + | ====Autoregulation==== |
+ | |||
+ | <center><big>'''Q = (PA - PE) ÷ R'''</big></center> | ||
+ | |||
+ | '''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 [[Reabsorption and Secretion Along the Distal Tubule and Collecting Duct - Anatomy & Physiology#Juxtaglomerular Apparatus| 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 [[Kidney - Blood Pressure - Anatomy & Physiology#Pressure Diuresis|pressure diuresis]]. | ||
+ | |||
+ | |||
− | + | ====[[Renin Angiotensin Aldosterone System|Angiotensin 2]]==== | |
− | + | ====[[Sympathetic Nervous System effect on Glomerular Filtration Rate|Sympathetic Nervous System]]==== | |
− | + | ====[[The Effects of Nitrous Oxide and Prostaglandins on GFR - Anatomy & Physiology|Nitrous Oxide and Prostaglandins]]==== | |
[[Category:Urinary System - Anatomy & Physiology]] | [[Category:Urinary System - Anatomy & Physiology]] |
Revision as of 17:59, 9 December 2010
Introduction
The glomerular filtration rate or GFR is the amount of fluid filtered from the capillaries into the Bowmans capsule per unit time. The GFR can be expressed as the following formula:
Kf = the filtration coefficent
Kf can furthermore be expressed by the following formula
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 = 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 = 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.