RENAL BLOOD FLOW

RENAL BLOOD FLOW

 The kidney are highly vascular organ and usually receive 1000 to 1200 ml of
blood per minute (20 – 25% of the cardiac output)
 About 600 -700 ml of blood flowing through the kidney per minute is plasma
(assuming HCT of 45% and plasma is 55%)
 From renal plasma flow (RPF), 20% (approximately 120 to 140 ml/min) is
filtered at glomerulus and passes into Bowman capsule
 The filtration of the plasma per unit of time is known as glomerular filtration rate
(GFR)
 The remaining 80% (about 480 ml) of plasma flows through the efferent
arterioles to the peritubular capillaries.
AUTOREGULATION

 This is the maintenance of renal plasma flow (RPF) despite changes in

systemic arterial pressure.
 The maintenance of RPF therefore ensure GFR is maintained.
 An increase in arterial pressure must therefore be accompany by an increase
in vascular resistance to maintained RPF at a constant level without changing
the pressure for filtration
 This is achieved mainly at the afferent arteriole.
 Increase BP (constrict afferent arteriole, dilate efferent arterole)
 Stable for BP range of 75 to 160 mmHG (cannot compensate for extreme BP
change)
Intrinsic : Myogenic mechanism

 Relies on inherent properties of the arterioles, themselves.

 Arteriole walls comprise smooth muscle, made of vascular smooth muscle
cells.
 When increased renal blood flow exerts increased hydrostatic capillary
pressure on the walls, stretch receptors are activated and induce
vasoconstriction.
 This reduces renal blood flow and, therefore, GFR.
 When renal blood flow is low, the stretch receptors are inactivated, and the
arteriole dilates to increase GFR.
Tubuloglomerular feedback
 This occur via the distal tubule and juxtaglomerular apparatus
 Relies on interaction between the nephron tubule and glomerulus.
 As renal blood flow increases, so does hydrostatic capillary pressure, and,
therefore, GFR increases.
 As the GFR increases, so does the concentration of salt in the ultrafiltrate,
because high flow rate allows less time for tubular reabsorption.
 The macula densa of distal tuble senses the high salt concentration in the
ultrafiltrate as it passes through the distal tubule;
 In response, it releases vasoconstrictor chemicals.
 Consequently, the nearby afferent arteriole constricts, which, as we saw
earlier:
Reduces renal blood flow, hydrostatic capillary pressure, and GFR.
 When renal blood flow decreases, so does the sodium concentration, and
eventually the macula densa stops releasing vasoconstrictors, which
ultimately allows renal blood flow and GFR to again increase.
EXTRINSIC : NEURAL PATHWAY

 Activated when mean arterial blood pressure drops below 80 mmHg.

 Sympathetic activation rapidly induces vasoconstriction of the arterioles to
the glomerulus to reduce GFR and to divert blood away from the kidneys to
support other body tissues
 This is particularly important in response to hemorrhage, in which loss of
blood volume lowers blood pressure, so blood is shunted away from the
kidneys to avoid body tissue necrosis.
Sympathetic Activation: Direct Effects

 Low blood pressure decreases carotid sinus activity.

 Cardiovascular centers of medulla in brainstem respond by releasing
norepinephrine via sympathetic nerves.
 Norepinephrine activates alpha 1 receptors on arterioles, initiates
vasoconstriction.
– Because afferent arteriole has more alpha 1 receptors, it constricts to a
greater degree.
– This reduces renal blood flow, hydrostatic capillary pressure, and GFR.
Extrinsic – Renin angiotensin system

 Activated when mean arterial pressure drops below 80 mmHg; recall that too-
low blood pressure can cause tissue necrosis
 To raise blood volume and pressure, the renin-angiotensin system produces
hormones that act on multiple organs, including the renal arterioles.
 One of these hormones, angiotensin II, has dose-dependent effects on GFR:
– At low levels, angiotensin II reduces renal blood flow but increases GFR.
– At higher levels, it reduces both renal blood flow and GFR.
 First, reduced renal blood flow induces the juxtaglomerular cells to
secrete renin, which is an enzyme.
 Within the blood stream, renin catalyzes the conversion
of angiotensinogen to angiotensin I, which is a hormone with only mild
vasoconstrictor effects.
 However, as it travels through the blood, *angiotensin-converting enzyme8
converts angiotensin I to angiotensin II.
 Angiotensin II has widespread effects throughout the body that raise blood
volume and pressure
Renin angiotensin
aldosterone system
 Angiotensin II induces arteriole vasoconstriction, especially of the 
efferent arteriole, which has more angiotensin-sensitive receptors than the
afferent arteriole does.
 Reduced blood flow through the efferent arteriole raises hydrostatic
capillary pressure within the glomerulus, which helps to maintain GFR within
the homeostatic range.
 However, if efferent arteriole blood flow is reduced too much, the 
oncotic capillary pressures overwhelm the hydrostatic pressures, and GFR is
reduced.
Renal Clearance

 Renal clearance is a measurement that is used to analyze and study the

function of the kidneys.
 Indicates whether a substance is filtered, reabsorbed, and/or secreted.
 It varies from one substance to another and it tells us how quickly a particular
substance is removed from the plasma by kidney and excreted in urine.
 The units of renal clearance is given in mL/min.
 For normal kidneys, the renal plasma flow is 625 mL/min while the
glomerular filtration rate is 125 mL/min.
 In order to measure GFR, a substance that will act as an appropriate marker
is needed that meets the following criteria
 Must be freely filtered across the glomerulus into Bowman space
 Must not be reabsorbed or secreted by the nephron
 Must not be metabolized or produced by kidney
 Must not alter GFR
 Two examples of GFR markers:

Inulin has a clearance exactly equal to GFR because it is filtered, but not
reabsorbed or secreted.

Creatinine has a clearance that is nearly equal to GFR because it is filtered
and only minimally secreted.
– However, since creatinine is an endogenous substance (and inulin is not), it
is the preferred GFR marker in most clinical situations.