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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
IntroductionGlomerular 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
ii. 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-
K ATPase 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
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
ReferencesGuyton 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
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