RENAL BLOOD CIRCULATION

INTRODUCTION
Blood vessels of kidneys are highly specialized to facilitate the functions
of nephrons in the formation of urine. The renal circulation supplies the
blood to the kidneys via the renal arteries, left and right, which branch
directly from the abdominal aorta. In the adults, during resting
conditions both the kidneys receive 1,300 mL of blood per minute or
about 26% of the cardiac output. Maximum blood supply to kidneys has
got the functional significance. Renal arteries supply blood to the
kidneys. The renal artery enters the kidney through the hilum and then
branches into segmental arteries, dividing further into interlobar arteries,
which penetrate the renal capsule and extend through the renal columns
between the renal pyramids. The interlobar arteries then supply blood to
the arcuate arteries that run through the boundary of the cortex and the
medulla.
Each arcuate artery supplies several interlobular arteries that feed into
the afferent arterioles that lead to the glomerular capillaries supply the
glomeruli, where large amounts of fluid and solutes are supplied. The
distal ends of the capillaries of each glomerulus coalesce (come together)
to form the efferent arteriole, which leads to a second capillary network
called the peritubular capillaries, that surrounds the renal tubules. The
renal circulation is unique in that it has two capillary beds, the
glomerular and peritubular capillaries, which are arranged in series and
separated by the efferent arterioles, which help regulate the hydrostatic
pressure in both sets of capillaries. High hydrostatic pressure in the
glomerular capillaries (60mmHg) causes rapid filtration, while a much
lower hydrostatic pressure in the peritubular capillaries (13mmHg)
permits fluid reabsorption. By adjusting the resistance of the efferent and
the afferent arterioles, the kidneys can regulate the hydrostatic pressure
in both the glomerulus and peritubular capillaries, thereby changing the
rate of glomerular filtration, tubular reabsorption or both in response to
body homeostatic demand. After filtration occurs, the blood moves
through a small network of venules that converge into interlobular veins,
as with the arteriole distribution, the veins follow the same pattern: the
peritubular capillaries empty into the arteriolar vessels and progressively
form the interlobular vein, arcuate vein, interlobar vein and the renal
vein, which leaves the kidney besides the renal artery and ureter. The
medullary interstitium is the functional space in the kidney beneath the
individual filters (glomeruli), which are rich in blood vessels. The
interstitium absorbs fluid recovered from urine. Various conditions can
lead to scarring and congestion of this area, which can cause kidney
dysfunction and failure.
RENAL BLOOD VESSELS

Renal Artery
Renal artery arises directly from abdominal aorta and enters the kidney through the
hilus. While passing through renal sinus, the renal artery divides into many
segmental arteries.
Segmental Artery
Segmental artery subdivides into interlobar arteries
Interlobar Artery
Interlobar artery passes in between the medullary pyramids. At the base of the
pyramid, it turns and runs parallel to the base of pyramid forming arcuate artery.
Arcuate Artery
Each arcuate artery gives rise to interlobular arteries.
Interlobular Artery
Interlobular arteries run through the renal cortex perpendicular to arcuate artery.
From each interlobular artery, numerous afferent arterioles arise.
Afferent Arteriole
Afferent arteriole enters the Bowman capsule and forms glomerular capillary tuft.
After entering the Bowman capsule, the afferent arteriole divides into 4 or 5 large
capillaries.
Glomerular Capillaries
Each large capillary divides into small glomerular capillaries, which form the loops.
And, the capillary loops unite to form the efferent arteriole, which leaves the
Bowman capsule.
Efferent Arteriole
Efferent arterioles form a second capillary network called peritubular capillaries,
which surround the tubular portions of the nephrons. Thus, the renal circulation
forms a portal system by the presence of two sets of capillaries namely glomerular
capillaries and peritubular capillaries.
Peritubular Capillaries and Vasa Recta
Peritubular capillaries are found around the tubular portion of cortical nephrons
only. The tubular portion of juxtamedullary nephrons is supplied by some
specialized capillaries called vasa recta. These capillaries are straight blood vessels
hence the name vasa recta. Vasa recta arise directly from the efferent arteriole of the
juxtamedullary nephrons and run parallel to the renal tubule into the medulla and
ascend up towards the cortex.
Venous System
Peritubular capillaries and vasa recta drain into the venous system. Venous system
starts with peritubular venules and continues as interlobular veins, arcuate veins,
interlobar veins, segmental veins and finally the renal vein. Renal vein leaves the
kidney through the hilus and joins inferior vena cava.

Direction of blood flow

Aorta - Arteries - Arterioles- Capillaries -Venule-Vein -Vena cava

Renal Blood Vessels
Renal Capillaries
Schematic diagram showing renal blood flow
MEASUREMENT OF RENAL BLOOD FLOW
Blood flow to kidneys is measured by using plasma clearance of para-aminohippuric
acid.
REGULATION OF RENAL BLOOD FLOW
Renal blood flow is regulated mainly by autoregulation. The nerves innervating renal
blood vessels do not have any significant role in this.
INNERVATION OF THE RENAL VESSELS
The kidney and nervous system communicate via the renal plexus, whose fibers course
along the renal arteries to reach each kidney. Input from the sympathetic nervous
system triggers vasoconstriction in the kidney, thereby reducing renal blood flow. The
kidney also receives input from the parasympathetic nervous system, by way of the
renal branches of the vagus nerve (cranial nerve X); the function of this is yet unclear.
Sensory input from the kidney travels to the T10-11 levels of the spinal cord and is
sensed in the corresponding dermatome. Thus, pain in the flank region may be referred
from corresponding kidney.
AUTOREGULATION

Autoregulation is the intrinsic ability of an organ to regulate its own blood flow. It is
present in some vital organs in the body such as brain, heart and kidneys. It is highly
significant and more efficient in kidneys.
Renal Autoregulation
one of the most striking characteristics of the renal circulation is the ability of the
kidney to maintain a constant renal blood flow (RBF) and glomerular filtration rate
(GFR) as renal perfusion pressure is altered. Renal autoregulation is important to
maintain the glomerular filtration rate (GFR). Blood flow to kidney remains normal
even when the mean arterial blood pressure vary widely between 60mmHg and 180
mmHg. This helps to maintain normal GFR. The dual regulation of both RBF and
GFR is achieved by proportionate changes in the preglomerular resistance and is
believed to be mediated by two mechanisms, tubuloglomerular feedback (TGF) and
the renal myogenic response.
 MECHANISMS INVOLVED IN RENAL
AUTOREGULATION
Two mechanisms are involved in renal autoregulation:
1. Myogenic response
2. Tubuloglomerular feedback.
1. Myogenic Response (MR)
The myogenic response involves a direct vasoconstriction of the afferent arteriole when this
vessel is presented with an increase in transmural pressure. Whenever the blood flow to
kidneys increases, it stretches the elastic wall of the afferent arteriole. Stretching of the vessel
wall increases the flow of calcium ions from extracellular fluid into the cells. The influx of
calcium ions leads to the contraction of smooth muscles in afferent arteriole, which causes
constriction of afferent arteriole. So, the blood flow is decreased. MR is a function of smooth
muscle to contract in response to external stretching force. In the case of vascular smooth
muscle, this causes vasoconstriction on a rise in arterial pressure thus allowing for
autoregulation.
2. Tubuloglomerular Feedback
Macula densa plays an important role in tubuloglomerular feedback, which controls the
renal blood flow and GFR. TGF involves a flow-dependent signal that is sensed at the
macula densa, and alters tone in the adjacent segment of the afferent arteriole via a
mechanism that remains controversial, but likely involves adenosine and/or ATP. Here the
kidney changes its own blood flow in response to changes in sodium concentration. The
sodium chloride levels in the urinary filtrate are sensed by the macula densa cells at the end
of the ascending limb. When sodium levels are moderately increased, the macula densa
releases ATP and reduces prostaglandin E2 release to the juxtaglomerular cells nearby. The
juxtaglomerular cells in the afferent arteriole constrict, and juxtaglomerular cells in both
the afferent and efferent arteriole decrease their renin secretion. These actions function to
lower GFR. Further increase in sodium concentration leads to the release of nitric oxide, a
vasodilating substance, to prevent excessive vasoconstriction. In the opposite case,
juxtaglomerular cells are stimulated to release more renin, which stimulates the renin-
angiotensin system, producing angiotensin I which is converted by Angio-Tensin
Converting Enzyme (ACE) to angiotensin II. Angiotensin II then causes preferential constriction of
the efferent arteriole of the glomerulus and increases the GFR.
 The current view is that these two mechanisms act in concert and that their
primary role is to stabilize renal function by preventing pressure-induced
fluctuations in RBF, GFR and the delivery of filtrate to the distal tubule (“distal
delivery”). Regulation of renal blood flow is important to maintaining a stable
glomerular filtration rate (GFR) despite changes in systemic blood pressure (within
about 80-180 mmHg).
MAJOR HORMONES THAT INFLUENCE GFR & RBF
The graph in the previous slide shows the autoregulation of GFR as mean arterial
blood pressure increases.
The overall speed of RBF autoregulation is crucial, because the kidney vasculature
is continuously challenged by fluctuations of pressure over a broad range of
frequencies from cycle length of seconds and minutes to hours and days. Since auto
regulation determines the amount of pressure fluctuations reaching the glomerulus,
peritubular capillaries and medullary circulation, its function is potentially
important for filtration, reabsorption, and pressure natriuresis and hypertensive renal
damage. Renal autoregulation minimizes the impact of changes in arterial blood
pressure on sodium excretion. Without renal autoregulation, increased in arterial
blood would lead to dramatic losses of sodium chloride and water from the ECF.
 SPECIAL FEATURES OF RENAL CIRCULATION
Renal circulation has some special features to cope up with the functions of the
kidneys. Such special features are:
1. Renal arteries arise directly from the aorta. So, the high pressure in aorta
facilitates the high blood flow to the kidneys.
2. Both the kidneys receive about 1,300 mL of blood per minute, i.e. about 26% of
cardiac output. Kidneys are the second organs to receive maximum blood flow, the
first organ being the liver, which receives 1,500 mL per minute, i.e. about 30% of
cardiac output.
3. Whole amount of blood, which flows to kidney has to pass through the
glomerular capillaries before entering the venous system. Because of this, the blood
is completely filtered at the renal glomeruli.
4. Renal circulation has a portal system, i.e. a double network of capillaries, the
glomerular capillaries and peritubular capillaries.
5. Renal glomerular capillaries form high pressure bed with a pressure of 60mmHg
to 70mmHg. It is much greater than the capillary pressure elsewhere in the body,
which is only about 25mmHg to 30mmHg. High pressure is maintained in the
glomerular capillaries because the diameter of afferent arteriole is more than that of
efferent arteriole. The high capillary pressure augments glomerular filtration.
6. Peritubular capillaries form a low pressure bed with a pressure of 8mmHg to
10mmHg. This low pressure helps tubular reabsorption.
7. Autoregulation of renal blood flow is well established.
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