Autoregulation of glomerular filtration rate and renal blood

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

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

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