Physiologic Control of Glomerular Filtration

and Renal Blood Flow

Determinants of GFR: glomerular hydrostatic pressure
and the glomerular capillary colloid osmotic pressure
Influenced by the sympathetic nervous system,
hormones and autacoids (vasoactive substances that
are released in the kidneys and act locally), and other
feedback controls that are intrinsic to the kidneys
Sympathetic Nervous System Activation
Decreases GFR
Strong activation of the renal sympathetic nerves can
constrict the renal arterioles and decrease renal blood
flow and GFR
Moderate or mild sympathetic stimulation has little
influence on renal blood flow and GFR
Hormonal and Autacoid Control
of Renal Circulation
Norepinephrine, Epinephrine, and Endothelin
Constrict Renal Blood Vessels and Decrease GFR
Norepinephrine and epinephrine (adrenal medulla)
have little influence on renal hemodynamics except
under extreme conditions, such as severe hemorrhage.
endothelin, is a peptide that can be released by
damaged vascular endothelial cells and increased in
certain disease states associated with vascular injury,
such as toxemia of pregnancy, acute renal failure and
chronic uremia

Angiotensin II Constricts Efferent Arterioles
angiotensin II preferentially constricts efferent
arterioles, increased angiotensin II levels raise
glomerular hydrostatic pressure while reducing renal
blood flow contributes to decreased flow through the
peritubular capillaries, which in turn increases
reabsorption of sodium and water
Endothelial-Derived Nitric Oxide Decreases
Renal Vascular Resistance and Increases GFR

Prostaglandins and Bradykinin Tend to Increase
GFR
Autoregulation of GFR and Renal
Blood Flow
Autoregulation:
Feedback
mechanisms
intrinsic to the
kidneys normally
keep the renal
blood flow and
GFR relatively
constant,

a change in arterial pressure exerts much less of an
effect on urine volume for two reasons: (1) renal
autoregulation prevents large changes in GFR, and
(2) additional adaptive mechanisms in the renal
tubules that allow them to increase their reabsorption
rate when GFR rises, a phenomenon referred to as
glomerulotubular balance
Role of Tubuloglomerular
Feedback
in Autoregulation of GFR
The tubuloglomerular feedback mechanism has
two components that act together to control GFR:
(1) an afferent arteriolar feedback mechanism and
(2) an efferent arteriolar feedback mechanism.

These feedback mechanisms depend on special anatomical
arrangements of the juxtaglomerular complex
Juxtaglomerular complex
Macula densa: is a specialized group of epithelial cells
in the initial portion of distal tubules that comes in
close contact with the afferent and efferent arterioles,
contain Golgi apparatus, which are intracellular
secretory organelles directed toward the arterioles,
suggesting that these cells may be secreting a
substance toward the arterioles.
Juxtaglomerular cells: in the walls of the afferent and
efferent arterioles

Decreased Macula
Densa Sodium
Chloride Causes
Dilation of
Afferent Arterioles
and Increased
Renin Release
Myogenic Autoregulation of Renal
Blood Flow and GFR
Another mechanism that contributes to the
maintenance of a relatively constant renal blood flow
and GFR is the ability of individual blood vessels to
resist stretching during increased arterial pressure, a
phenomenon referred to as the myogenic
mechanism.
Regulation of Tubular Reabsorption
Glomerulotubular BalanceThe Ability of the
Tubules to Increase Reabsorption Rate in
Response to Increased Tubular Load
The normal rate of peritubular capillary reabsorption
is about 124 ml/min
Reabsorption = Kf x Net reabsorptive force
Net reabsorption pressure is 10 mm Hg,
Kf normally is a measure of the permeability and
surface area of the capillariesabout 12.4 ml/min/mm
Hg.
Summary of the hydrostatic and colloid osmotic forces
that determine fluid reabsorption by the peritubular
capillaries.
Regulation of Peritubular Capillary Physical Forces
The peritubular capillary hydrostatic pressure is
influenced by the arterial pressure and resistances of
the afferent and efferent arterioles.

Effect of Arterial Pressure on Urine OutputThe
Pressure-Natriuresis and Pressure-Diuresis
Mechanisms
Even small increases in arterial pressure often cause
marked increases in urinary excretion of sodium and
water, phenomena that are referred to as pressure
natriuresis and pressure diuresis
Hormonal Control of Tubular Reabsorption
Sympathetic Nervous System Activation Increases
Sodium Reabsorption
Sympathetic activation also increases sodium
reabsorption in the proximal tubule, the thick
ascending limb of the loop of Henle, and perhaps in
more distal parts of the renal tubule.
sympathetic nervous system stimulation increases
renin release and angiotensin II formation, which adds
to the overall effect to increase tubular reabsorption
and decrease renal excretion of sodium.