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Autoregulation of glomerular filtration rate
and renal blood flow
Prepared by:
Deepa Devkota
Roll no:07
Human Biology 7th batch
Overview
 Introduction:
 Glomerular filtration rate
 renal blood flow
 Autoregulation of GFR and renal blood flow
 Tubuloglomerular feedback mechanism
 Myogenic autoregulation
 Importance of Autoregulation
Introduction
Glomerular filtration rate (GFR):
 Rate at which plasma is filtered from the glomerular capillaries into
bowman’s capsule per unit time.
 In average, GFR is about 125ml/min or 180 l/day and filtration
fraction is about 0.2(20%)
Renal blood flow
• In an average 70 kg man: renal blood flow is about 1100ml/min
(22% of cardiac output)
• To supply enough plasma for high rate of glomerular filtration for the
precise regulation of body fluid volumes and solute concentration
• Renal blood flow= renal artery pressure-renal vein pressure
total renal vasculature resistance
• Renal arterial pressure is about equal to systemic arterial pressure but
the pressure of renal veins averages about 3-4 mm Hg
• Most of the renal vascular resistance resides in interlobular arteries,
afferent and efferent arterioles.
Autoregulation of GFR and renal blood flow
• Effective intrinsic feedback mechanism for the maintenance of renal
blood flow and GFR despite marked change in arterial blood pressure
• Relatively constant over an arterial pressure range between 80 and
170 mm Hg
Tubuloglomerular feedback mechanism
• Links the change in sodium chloride concentration at macula densa
with the control of renal arteriolar pressure
• Helps to ensure a relatively constant delivery of sodium chloride to
distal tubule and helps to prevent spurious fluctuation in renal
excretion.
• Has two components that act together to control GFR:
i. Afferent arteriolar feedback mechanism
i. Efferent arteriole feedback mechanism
Efferent arteriole feedback mechanism
Decrease in
arteriolar blood
pressure causes
decrease in GFR
slows flow rate
in loop of henle
causing increased
reabsorption of
Na and Cl in
ascending loop of
henle
Reduced NaCl
in macula
densa causes
paracrine
diffusion of
renin from
granular cells
of the JGA
Conversion of
angiotensinogen
to angiotensin-I
Angiotensin I is
converted to
angiotensin II by
angiotensin
converting enzyme
Efferent arteriole
vasoconstriction
causing increase in
glomerular
hydrostatic
pressure
Contd…
• Angiotensin II act on adrenal gland to release aldosterone
• Aldosterone stimulates the epithelial cells of the distal tubule and
collecting ducts of kidney to increase reabsorption of sodium in
exchange of potassium
• RAS act on CNS for the secretion of vasopressin(ADH) from
posterior pituitary gland to increase water intake by stimulating thirst,
reduce urinary loss by concentrating urine
Contd..
• The afferent and efferent arterioles are innervated by sympathetic
neurons .
• Norepinephrine is released by sympathetic nerve and circulating
epinephrine by adrenal medulla, causing vasoconstriction by binding
to α1 adrenoreceptor.
• Macula densa cells also secrete nitric oxide which puts brake on the
action of ATP and adenosine at afferent arteriole
Afferent arteriole feedback mechanism
Increase in GFR
secondary to
increase in
arteriole
pressure
More NaCl enter
the macula
densa cells via
the Na–K–2Cl
cotransporter in
their apical
membranes
increased Na+
causes increased
Na- KATPase
activity which
results increased
ATP hydrolysis
causing more
adenosine to be
formed
Adenosine acts via
adenosine A1
receptors to increase
release of Ca2+ to the
vascular smooth
muscle of the
afferent arterioles.
Afferent
vasoconstriction
causing
decreased GFR
Adjustment in renal arteriole caliber to
alter GFR and renal blood flow
Tubuloglomerular feedback mechanism
Myogenic autoregulation of renal blood flow
and GFR
• Ability of individual blood vessels(small arterioles) to resist wall
stretching during increased arterial pressure
Vascular Wall
stretch
Increased
movement of
calcium from
ECF into cells
Contraction of
vascular smooth
muscle
prevention
of excessive
stretch of
the vessels
Increase in
vascular
resistance
Prevents
excessive
increase in GFR
and renal blood
flow
Contd..
• this pressure sensitive mechanism has no direct means of detecting
change in renal blood flow and GFR
• May be important in protecting kidney from hypertension induced
injury
Importance of Autoregulation in preventing
extreme change in renal excretion
• In the absence of autoregulation, an increase of blood pressure (from
100 to 125 mm Hg ) would cause about 25% increase in
GFR(180l/day to 225l/day)
• If the tubular reabsorption remained constant, it causes an increase in
urine flow to 46.5l/day (30 folds increase)
• Since plasma volume is only about 3l, it causes quick depletion of
blood volume
• Even with these special control mechanism, change in arterial
pressure have significant effect on renal excretion of water and
sodium known as pressure natriuresis or pressure diuresis
References
Guyton and hall, textbook of medical physiology,12th
edition
Johnson Leonard R., essential medical physiology,3rd
edition
William F. Ganong ,review of medical physiology ,23rd
edition
Bern and Levy,physiology,5th edition
Autoregulation of glomerular filtration rate and renal blood

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Autoregulation of glomerular filtration rate and renal blood

  • 1. Autoregulation of glomerular filtration rate and renal blood flow Prepared by: Deepa Devkota Roll no:07 Human Biology 7th batch
  • 2. Overview  Introduction:  Glomerular filtration rate  renal blood flow  Autoregulation of GFR and renal blood flow  Tubuloglomerular feedback mechanism  Myogenic autoregulation  Importance of Autoregulation
  • 3. Introduction Glomerular filtration rate (GFR):  Rate at which plasma is filtered from the glomerular capillaries into bowman’s capsule per unit time.  In average, GFR is about 125ml/min or 180 l/day and filtration fraction is about 0.2(20%)
  • 4. Renal blood flow • In an average 70 kg man: renal blood flow is about 1100ml/min (22% of cardiac output) • To supply enough plasma for high rate of glomerular filtration for the precise regulation of body fluid volumes and solute concentration • Renal blood flow= renal artery pressure-renal vein pressure total renal vasculature resistance • Renal arterial pressure is about equal to systemic arterial pressure but the pressure of renal veins averages about 3-4 mm Hg • Most of the renal vascular resistance resides in interlobular arteries, afferent and efferent arterioles.
  • 5. Autoregulation of GFR and renal blood flow • Effective intrinsic feedback mechanism for the maintenance of renal blood flow and GFR despite marked change in arterial blood pressure • Relatively constant over an arterial pressure range between 80 and 170 mm Hg
  • 6. Tubuloglomerular feedback mechanism • Links the change in sodium chloride concentration at macula densa with the control of renal arteriolar pressure • Helps to ensure a relatively constant delivery of sodium chloride to distal tubule and helps to prevent spurious fluctuation in renal excretion. • Has two components that act together to control GFR: i. Afferent arteriolar feedback mechanism i. Efferent arteriole feedback mechanism
  • 7.
  • 8. Efferent arteriole feedback mechanism Decrease in arteriolar blood pressure causes decrease in GFR slows flow rate in loop of henle causing increased reabsorption of Na and Cl in ascending loop of henle Reduced NaCl in macula densa causes paracrine diffusion of renin from granular cells of the JGA Conversion of angiotensinogen to angiotensin-I Angiotensin I is converted to angiotensin II by angiotensin converting enzyme Efferent arteriole vasoconstriction causing increase in glomerular hydrostatic pressure
  • 9. Contd… • Angiotensin II act on adrenal gland to release aldosterone • Aldosterone stimulates the epithelial cells of the distal tubule and collecting ducts of kidney to increase reabsorption of sodium in exchange of potassium • RAS act on CNS for the secretion of vasopressin(ADH) from posterior pituitary gland to increase water intake by stimulating thirst, reduce urinary loss by concentrating urine
  • 10. Contd.. • The afferent and efferent arterioles are innervated by sympathetic neurons . • Norepinephrine is released by sympathetic nerve and circulating epinephrine by adrenal medulla, causing vasoconstriction by binding to α1 adrenoreceptor. • Macula densa cells also secrete nitric oxide which puts brake on the action of ATP and adenosine at afferent arteriole
  • 11. Afferent arteriole feedback mechanism Increase in GFR secondary to increase in arteriole pressure More NaCl enter the macula densa cells via the Na–K–2Cl cotransporter in their apical membranes increased Na+ causes increased Na- KATPase activity which results increased ATP hydrolysis causing more adenosine to be formed Adenosine acts via adenosine A1 receptors to increase release of Ca2+ to the vascular smooth muscle of the afferent arterioles. Afferent vasoconstriction causing decreased GFR
  • 12. Adjustment in renal arteriole caliber to alter GFR and renal blood flow
  • 14. Myogenic autoregulation of renal blood flow and GFR • Ability of individual blood vessels(small arterioles) to resist wall stretching during increased arterial pressure Vascular Wall stretch Increased movement of calcium from ECF into cells Contraction of vascular smooth muscle prevention of excessive stretch of the vessels Increase in vascular resistance Prevents excessive increase in GFR and renal blood flow
  • 15. Contd.. • this pressure sensitive mechanism has no direct means of detecting change in renal blood flow and GFR • May be important in protecting kidney from hypertension induced injury
  • 16. Importance of Autoregulation in preventing extreme change in renal excretion • In the absence of autoregulation, an increase of blood pressure (from 100 to 125 mm Hg ) would cause about 25% increase in GFR(180l/day to 225l/day) • If the tubular reabsorption remained constant, it causes an increase in urine flow to 46.5l/day (30 folds increase) • Since plasma volume is only about 3l, it causes quick depletion of blood volume • Even with these special control mechanism, change in arterial pressure have significant effect on renal excretion of water and sodium known as pressure natriuresis or pressure diuresis
  • 17. References Guyton and hall, textbook of medical physiology,12th edition Johnson Leonard R., essential medical physiology,3rd edition William F. Ganong ,review of medical physiology ,23rd edition Bern and Levy,physiology,5th edition