Renal
system
Factors
Measurements
Renal blood
Nephrons
Glomerular
Functions
affecting
ofcapillary
supply
kidney
of GFR
GFRmembrane
and RBF
Kidney consists of 8-10 conical pyramids, bases in
outer =cortex,
apices
toward
pelvis,
medulla
subdivGFR
Structural
Kf *&filtration
(net
functional
ultrafiltration
units,
more
pressure)
than million,
in
Measurement
RBF:
increases
ofGFR
RBF
Glomerular
GFR
rate
﴾GFR﴿
Regulation
Substance
Three
layers:
used
of
capillary
ECF
to
measure
vol.,
endothelium,
osmolarity
GFR
&
&
RBF
BM
composition,
must:
&
visceral
supplies
renal
﴿
1.25
L\min
﴾
25%
of
cardiac
output
idedincreases
into
&(Cx)
zones,
outer
zone
into outer
each
kidney,
=clearance
Kfouter
* (PG
composed
+inner
ΠB=–of
PB
the
- –ΠG)
following
structures:
RBF
FF:
=
RPF
\(creatinine)
(1-hematocrit)
GFR
Endogenous
or
exogenous
(inulin)
Renal
GFR
TR
+
TS
regulation
1.
layer
Not
of
be
Bowman's
toxic.
of
BP,
acid-base
capsule
(podocytes).
balance,
bone
metaboli.RPF
Renal
artery,
﴿
97%
﴾
tissue,
greater
flow
to
cortex
GFR
=
RPF
*
FF
&
inner
stripes,
pyramid
pours
urine
into
minor
Glomerulus:
=
Kf
*
(60
globular
+
0
–
18
tuft
32)
of
capillaries,
respectively
afferent
Cortical
renal
nephrons:
blood
flow
70%-80%,
﴾RBF
﴿*
outer
(1-hematocrit)
two
thirds
of&
When
Vasoconstriction
x is used
100%toextracted
ofmeasure
afferentfrom
arterioles
plasma&
decreases
excreted;
substance
GFR.
sm
2.
but
Not
(excretion
﴾
Endothelial
be
stored,
of
calcium
or
layer:
metabolized
fenestrated,
&
phosphate
by
kidney.
even
ions
proteins
&
segmental,
interlobar,
arcuate
arteries,
interlobular
GFR
=
glomerular
filtration
rate
of
x
calyx,
every
2-3
calyces
unite
toPrenal
form
major
calyx
efferent
=
Kf
arteriole,
*tAHL,
(+10
mmHg)
inside
Bowman's
capsule,
Bd
is
cortex,
no
efferent
narrower
than
afferent.
its
GFR
extraction
(decreased
ratio
PG)
E
=
1.0
&
its
clearance=
C
FF
=
filtration
GFR
=
fraction,
C
=
U
RPF
*
V
=
\
plasma
flow
x
x
in ﴿secreted
in art.s
in
=
1250
ml\min
*
0.5
formation
3.
can
Not
pass.
be
produced,
﴿
not
1,
25
cells
dihydroxycholecalcipherol),
or
reabsorbed
by
produ,Kf=ultrafiltration
afferent
arterioles
radial
or
medullary
rays
﴾
which
unites
with
other
major
calyces
to
form
renal
filtered
&
transferred
coefficient
to
renal
(=surface
tubules:
area*capillproximal
Juxtamedullary
nephrons:
inner
third
of
cortex,
RPF
Slight
=tubular
vasoconstriction
CxC\ inEx==reabsorption
Cx \ 1.0 of
=C
efferent
arterioles
Where
Clearance
of
inulin
TR
=
of
x
x
ction
renal
>100
times
of
tubules.
erythropoietin
other
capillary
hormone,
﴾
BM:
high
excretion
permeability,
of
&
glomerular
capillaries,
efferent
arterioles
,
periGFR
=
625
ml\min
*
20%
pelvis
that
leads
urine
through
ureter
which
ary
tubule(PCT
permeability),
or
pars
P=hydrostatic
convoluta&
PST
pr.,
Π=smotic
or
pars
recta)
pr.
long
tAHL,
=
625
ml\min
efferent
wider
than
afferent.
Substance
increases
GFR
(x)
is
(increased
not
found
PG)
yet.
Instead,
substance
U
=
Urinary
concentration
of
inulin
in GFR or
.of
various
4.
﴿
membranes
Not
affect
metabolic
waste
RBF
products,
by
itself.
drugs,
toxic
tubular
capillaries,
(vasa
recta,)
interlobular
veins,
TS
=
tubular
secretion
of
x
emerges
through
hilum
of
kidney
from
which
,Severe
distal
colloids,
tubule,
B=inside
JGA,
Bowman's
﴿
TAHL
﴾
,
﴿
tAHL
capsule,
﴾
,
﴿
tDHL
G=inside
﴾renal
,
called
paraaminohippuric
vasoconstriction
of acid
efferent
(PAH)
arterioles
its extraction
GFR
=
125
V
ml\min
=
Urine
flow
substances
Other
filtered
&
poisons.
materials
&
ions
pass
easily
through
arcuate,
interlobar,
segmental
and
renal
veins.
arteryiscollecting
enters
&
renal
vein
leaves.
Ureters
pour
into
glomerular
DCT,
capillaries.
tubules,
These
collecting
are
Starling
tubes,
cortical
forces
&
ratio
decreases
0.9
GFR
(E
(increased
=
0.9)
ΠG)
P
=
Plasma
concentration
of
inulin
in& PAH
membrane
slit
pores
between
feet
of
podocytes.
urinary
fromduct,
which
urethra
emerges.
medullary
CD, main
minor
& major
calyx.
RPF
= Cbladder
PAH \ EPAH = CPAH \ 0.9
Exit
BASIM ZWAIN LECTURE NOTES
Home
Renal
system
Tubular
Factors
Control
Body
Regulation
control
affecting
of
reabsorption
GFR
tubular
ofof
ECF
blood
ECF
tubular
reabsorption
osmolarity
volume
osmolarity
reabsorption
and pressure
Countercurrent
mechanism
+ reabsorption
When
GFR
is
decreased;
tubular
flow
slows
down,
1Sympathetic
activity:
increases
Na
Highly
B-Angiotensin-II:
selective
process,
Produced
passive
by
lungs
or
active,
from
Some
4TR
Human
Plasma
= Kfosmolarity
body
* levels
(netmust
reabsorption
of amino
getosm
rid
acids
of pressure)
not&less
glucose:
than
600
tubular
Plasma
(P
)
calculated
from
plasma
1-Sympathetic
nervous
activity:Strong
sympathetic
Many
There
DThirst
Atrial
substances
is
center
glomerulotubular
natriuretic
in
brain
are
peptide
reabsorbed
stem
balance,
increases
(ANP):
along
when
Produced
the
with
desire
GFR
other
by
for
increased
tubular
reabsorption
of
NaCl,
decrease
b.Myogenic
mechanism:
Increased
RBF
that
causes
2Hormonal
activity:
3-Autoregulation:
According
Descending
Osmoreceptor
to
&
equation,
ascending
cells
lie
in
when
limbs
anterior
no
of
conc.
Henle's
hypothalamus
urine;
loop
the
and
&
substances
angiotensin-I
completely
(produced
reabsorbed:
in
liver
from
aa
angiotensino&
glucose,
Tm
About
of
glucose(TmG)
15%
of
water
reabsorption
is
about
325
mg\min,
occurs
in
its
tDHL
ideal
reabsorption
mosm
=
Kf
of
metabolic
*
(Pif
of
–
amino
Pc
wastes
+
Πc
acid
per
Πif)
and
day.
glucose
So,
it
is
is
unlimited
very
Starting
The
Remaining
Small
major
increase
from
active
reabsorption
tAHL,
in
reabsorption
Bd
vol.,
all
the
processes
large
following
of
increase
electrolytes
of
electrolytes
segments
in
CO....
are
+ conc.
sodium
(P
+GFR
)….
P
=
2.1
*
P
+
activity
decreases
e.g.,
in
severe
hemorrhage
Urea
recirculation
is
responsible
for
about
40%
of
Na
osm
Na
Na
intake
ECF
volume
Blood
pressure
substances
increases;
cardiac
water
intake
atria
tubular
like
&
in
chloride
increase
response
reabsorption
ions
secretion
to
any
which
increases.
increase
of
follow
ADH.
in
sodium
But
Thirst
Bd
vol.
Chronic
increase
in
BP
is
balanced
by
decrease
in
+
NaCl
near
osmoreceptors,
macula
densa
send
increase
in
GFR;
at
the
same
time
causes
distension
A-Aldosterone:
adrenal
cortex,
acts
on
principal
a.Juxtaglomerular
minimum
vasa
sensitive
recta
to
obligatory
run
any
long
increase
feedback
distance
urine
in
Na
volume
parallel,
mechanism:
conc.,
will
counter
send
increase
Juxtaglosignals
&
in
1-Sympathetic
Ability
of
kidney
nervous
to
conc.
activity
urine
requires
presence
of
some
gen
or
are
called
mostly
renin).
reabsorbed:
Renin
is
formed
bicarbonates
in
kidneys.
&
some
It
renal
which
threshold
is
carried
is
back
325\125
to
the
=2.6
systemic
mg\ml
circulation
=
260
mg\dL
via
1-Osmoreceptors-ADH
feedback
,Small
necessary
when
=
Kf
plasma
*
to
(6
excrete
–
levels
13
+
32
not
of
–
amino
less
15)
than
mmHg
acids
0.5
and
respectively
liters
glucose
of
highly
impermeable
occurs
(about
increase
5%)
in
TAHL
occur
to
in
water
(about
CO,
in
distal
large
in
30%)
absence
segments.
increase
which
of
ADH
is
in
Net
mainly
BP..
result
but
Small
very
due
is
The
major
bulk
of
tubular
reabsorption
of
water
&
But,
in
patients
with
renal
diseases,
plasma
conc.s
Normal
ECF
osmolarity
is
about
280-300
mosm\L
&
cerebral
ischemia
while
role
of
parasympathetic
the
process
of
urine
concentration
when
urea
is
ions,
active
center
acts
sodium
transport
is
especially
also
chloride
stimulated
processes
on
collecting
salt
by
which
may
decreased
ducts
be
follows
saturated
to
ECF
decrease
water.
volume,
when
+
angiotensin
II
production
results
in
decrease
impulses
to
JG
cells
to
relax,
vasodilatation
of
of
afferent
arterioles
and
stretch
of
smooth
muscles
cells
of
distal
tubules,
increase
Na
reabsorption
&
merular
resulting
close
to
supraoptic
proximity
apparatus
in
excessive
nuclei
to
each
(JGA):
to
loss
stimulate
other.
of
specific
body
Descending
posterior
fluids
distal
(diabetes
tubular
limbs
pituitary
are
2-Hormones
hyperosmotic
and
medulla
autacoids
created
by
countercurrent
electrolytes,
acts
directly
some
(or
indirectly
are
mostly
after
reabsorbed
stimulation
in
the
of
But
ascending
actual
vasa
renal
recta.
threshold
But
tDHL
for
glucose
is
impermeable
is
about
180
to
2-Thirst
center
in
brain
stem
increase;
concentrated
=
Kf
*
tubular
(+10
urine
mmHg)
reabsorption
daily:
increase,
decreased
Angiotensin
II
Baroreceptors
little
to
hyperosmotic
increase
1Na+-2Cl¯-1K+
amounts
in
BP,
medulla
of
large
solutes
active
increase
which
are
cotransport
passively
favours
in
urine
further
reabsorbed
process
excretion.
water
in
solutes
(about
65%)
occurs
in
proximal
tubules.
So,
of
urea
&
glucose
are
also
calculated.
and
it
is
mostly
dependant
on
sodium
ions
conc.
+
(vagal)
innervations
is
yet
unknown.
reabsorbed
from
medullary
colleting
tubules
to
the
Some
tubular
sodium
decreased
substances
and
lumen
BP,
water
angiotensin
overloaded.
50%
reabsorption
reabsorbed
II
Maximum
&
dryness
and
(50%
so,
tubular
increase
of
excreted)
mouth,
load
+ excretion.
Na
reabsorption
directly
or
indirectly
by
decreasafferent
arterioles,
increase
Bd
flow
to
glomerular
lining
their
walls.
This
stretch
results
in
myogenic
K
It
increases
permeability
of
luminal
epithelial
insipidus).
called
gland
to
countercurrent
increase
cells
Excessive
(macula
secretion
intake
multipliers
densa:
of
of
ADH
hyperosmotic
osmoreceptors,
because
(vasopressin)
they
fluids
to
3-Autoregulation
mechanism
&
urea
recirculation
&
ADH.
presence
aldosterone)
of
hormones:water
to
increase
sodium
reabsorption
ions
reabsorption.
increases
mg\dL,
solutes
which
this
difference
stay
within
may
thin
be
segment
due
to
that
not
not
all
of
3-Salt
appetite
center
in
brain
stem
amounts
Kf
is
constant
NaCl
depends
near
osmoreceptors
on
surface
area,
of
thickness
macula
&
tAHL.
which
reabsorption
Acute
increase
works
So,
tubular
against
(about
in
BP
fluid
19%)
as
balanced
much
reaches
from
as
by
collecting
the
200
direct
following
mosm\L
increase
ducts
conc.
in
in
tubular
fluid
reaches
the
thin
segments
within
its
When
P
decreases;
excretion
of
large
amounts
of
(142
mEq\L).
Normal
daily
sodium
ions
intake
2-Hormones&autacoids:Adrenaline,
noradrenaline
medullary
interstitium
to
be
secreted
again
from
+
osm
like
just
urine
pharynx
urea.
before
excretion
&
Some
saturation
esophagus
to
substances
restore
is
&
transport
vice
normal
completely
versa.
Bd
maximum
Inhibited
vol.
excreted
(Tm).
also
like
+
+
+
ing
aldosterone
production
from
adrenal
cortex.
capillaries,
increase
GFR
&
vice
versa
contraction
of
smooth
muscles
&
vasoconstriction
600
mosm\day
Na
excretion
Pressure
natriuresis
Brain
stem
membrane
to
Na
&
stimulates
Na
-K
pump
in
sensitive
like
continuously
increase
sea
water
water
to
changes
bring
will
reabsorption.
seriously
new
in
conc.
NaCl
increase
of
ADH
to
NaCl)
medulla
is
P
stimulated
in
contact
while
&
min.
by
4-Plasma
levels
of
amino
acids
and
glucose
+
in
C-Antidiuretic
presence
of
antidiuretic
hormone
(vasopressin):
hormone,
sodium
produced
ions
renal
reabsorbed.
tubules
So,
have
tubular
the
same
fluid
Tm
reaches
and
that
the
ascending
some
of
osm
densa,
permeability,
send
impulses
P
is
hydrostatic
to
JG
cells
pr.,
to
Π
relax
is
osmotic
resulting
pr.
segment
gradient.
presence
Na
excretion
still
of
So,
ADH
hyperosmotic
tubular
due
&
to
only
increase
fluid
about
reaches
(900
GFR
1%
mosm\L).
distal
&
of
decrease
filtered
tubules
water
in
original
osmolarity
(300
mosm\L).
diluted
urine
(down
to
50
mosm\L)
while
when
P
must
equals
its
daily
output
=
10-20
mEq
,by
angiotensin
II,
aspirin&
endothelin
decrease
GFR.
the
tubular
cells
of
thin
segments
to
their
lumen
osm
creatinine
Maximum
E-Parathyroid
gastric
distension.
and
plasma
some
hormones:Produced
conc.
drugs
before
and
poisons.
a
substance
by
parathyroid
starts
to
=
0.5
L\day
this
is
the
minimum
obligatory
urine
volume
Renin
is
also
produced
by
JG
cells
in
response
to
of
afferent
arterioles
&
decreased
RBF
&
GFR.
basolateral
membrane.
Adrenal
insufficiency
with
obligatory
ascending
decreased
specific
Bd
vasa
urine
smooth
vol.,
recta
vol.
decreased
muscle
even
are
called
with
cells
BP,
maximum
countercurrent
nausea,
in
wall
of
vomiting,
urine
afferent
+filtered
+acts
reabsorption
from
posterior
in
pituitary
presence
gland
of
aldosterone
and
it
and\or
on
distal
the
limbs
highly
glucose
hyperosmotic
molecules
(1200
before
mosm\L).
Tm
bypass
in
of
colloids,
vasodilatation
c
is
peritubular
of
afferent
arterioles,
capillaries,
increase
and
if Bd
isto
hypoosmotic
excreted
Na
reabsorption
in
urine.
(100
with
While
mosm\L).
increase
in
absence
in
Na
of
ADH,
leak
back
about
increases;
excretion
of
small
amounts
of
highly
1200
mosm\L
Nitric
oxide,
prostaglandin
&
bradykinin
increase
where
the
cycle
is
repeated
again
and
again.
appear
glands
Salt
appetite
&
in
act
urine
center
especially
its
in
renal
the
on
brain
TAHL
threshold=Tm\GFR
stem
(&
DCT)
increases
the
+ to
increase
in
GFR
or
RBF,
production
of
angiotensin
(Addison's
disease)
results
in
excessive
Na
loss
&
arterioles,
conc.
exchangers
morphine
resulting
&
juxtaglomerular
because
nicotine
in
death
they
&
from
vice
continuously
cells.
versa.
dehydration.
ADH
draw
inhibited
back
+
angiotensin
and
collecting
II
tubules
hormones.
and
ducts
to
increase
water
reabsorption.
flow
interstitial
to
glomerular
fluid
capillaries,
increase
GFR.
20%
tubular
of
filtered
lumen
(pressure
water
is
excreted.
natriuresis)
which
is
Aldosterone
Na
reabsorption
Sympathetic
activity
conc.
urine
(up
to
1200
mosm\L).
GFR
increase
desire
for
calcium
salt
intake.
and
magnesium
ions
reabsorption
+
IK
&
angiotensin
II
to
decrease
GFR
&
RBF.
retention
while
adrenal
hyperactivity
(Cushing
water
by
alcohol
from
intake.
medulla
to
the
systemic
circulation.
reabsorption
and
urine
concentration.
always
accompanied
by
pressure
diuresis
and
decrease
phosphate
+reabsorption.
+ depletion
syndrome)
results
in
Na
retention
&
K
Home
Exit
BASIM ZWAIN LECTURE NOTES
Renal
system
Body regulation
Physiology
of micturition
of acid-base balance
Urine
enters
bladder
in
spurts
synchronous
with
+] will
Buffer
The
first
internal
systems:
urge
urethral
to
void
is
sphincter,
felt
at all
volume
smooth
ofmuscles
150
ml
&
on
Any
change
in
[H
affect
cellular
and
body
2-Phosphate
buffer
system:
important
buffer
in
regular
peristaltic
contractions
ofacidic
ureteric
smooth
1-Bicarbonate
the
either
marked
sides,
sense
plays
buffer
of
no
fullness
role
system:
inonmicturition,
ismany
the
at
400
most
ml.
important
in
But
male
thisitis
c.
Renal
regulation:
excretion
of
or
alkaline
functions
due
to
its
effects
reactions.
intracellular
&
renal
tubular
fluids.
Its
pK
is
6.8
+
When
4-Ammonium
Respiratory
HCO
regulation:
¯
buffer
decreases;
system:
stimulation
metabolic
the
last
acidosis
of
choice
respiratory
system
+
muscles
(1-5/minute),
of
ureters
+property
3renal
buffer
relieved
prevents
system
by
retrograde
inECF
ECF.
ejaculation
ofoblique
when
plasticity.
[Hinsertion
](reflux
isis
Micturition
increased:
semen
isso; it
urine.
Daily
secretion
of
H
4400
mmol.
Normal
[H
]
in
is
only
0.00000004
mol\L,
+
2
When
[H+]
increases:
H
+
HPO
¯
→
H
PO
¯
4
2
4
+
¯
When
in
center
renal
PCO
bytubules
central
increases;
when
chemosensitive
bicarbonate
respiratory
areas
and
acidosis
which
phosphate
areof
into
vicinity
of
bladder
walls
prevents
back
flow
+](expired)
2
H
initiated
+HCO
urinary
after
→
bladder).
relaxation
H
CO
External
→
of
H
muscles
O
+
sphincter,
CO
of
pelvic
skeletal
floor,
Bicarbonates
system
buffers
4320
mmol
&
other
80
is
better
to
use
pH
(which
is
–log
[H
=
7.4).
3
2
3
2
2
When
[OH¯]
is
increased:
When
systems
bilateral
HCO
are
aggregations
saturated.
¯
increases;
of
Ammonium
neurons
metabolic
beneath
is
alkalosis
formed
ventral
from
urine.
Bladder
parasym.:S2,
S3&
S4
with
pelvic
nn.
3
While
downward
muscle,
when
contracts
pull
[OH-]
on
voluntarily,
detrusor
is
increased:
muscle,
delay
micturition
excitation
ofor
mmol
buffered
by
phosphates
&
then
ammonium
Nobody
can
survive
more
than
hours
when
pH
2
OH¯
+
H
PO
¯
→
HPO
¯
+
H
O
+&P
2
4
4
2
When
metabolism
surface
PCO
of
medulla
of
decreases;
glutamine
sensitive
respiratory
inside
to
changes
renal
alkalosis
tubular
in
H
cells.
Sym.
from
L1,
L2
&L3
via
hypogastric
nn
after
+
2
CO2
OH¯
stretch
interrupt
+
receptors
HMost
its
CO
starting.
→
in
H
its
O
Delay
wall,
+
HCO
micturition
reflex
¯
(excreted)
contraction.
is
learning
The
systems.
renal
tubular
cells
utilize
secondary
raises
to
8.0
or
falls
to
6.8
Regulation
of
[H
]
is
by
2
3
2
3
3-Protein
buffer
systems:the
most
available
intra+ + NH
++& raises
When
Double
[H+]
alveolar
increases:
ventilation
H
reduces
→
NH
P
+
+
relay
intransport
ganglion.
3micturition;
CO2
4 for
The
afferent
ability
power
ofinferior
&brain
efferent
ofofdissociation
inmesenteric
adults.
limbs After
of
constant
voiding
(pK)
reflex
run
female
thiswith
active
to
secrete
H
like
Na
-H
antiport,
one
or
more
the
following
systems:
Chemical
cellular
systems
but
also
work
the
th extracellularly.
When
pH
from
[OH-]
7.4
to
is
7.63
increased:
while
1\4
OH¯
alveolar
+
NH4+
ventilation
→
NH4OH
Somatic
sensory
& motor
from
S2,
S3 &
S4
viaby
system
pelvic
urethra
nerves
is
empties
6.1,
to
so sacral
Henderson-Hasselbalch
by
gravity
cord,
while
threshold
male
is
urethra
adjusted
equation:
but
the
intercalated
cells
of
distal
tubules
utilize
acid-base
buffer
systems
in
body
fluids,
respiratory
most
important
is
hemoglobin
in
RBCs.
raises
Pcontractions
& facilitatory
reduces
pH
tovia
6.95
pudendal
nn.
Sensory
also
pelvic
&
hypogastric
CO2
pH
by
several
=renal
6.1
+
of
log
[HCO
of
¯]\0.03
bulbocavernosus
(pons
PCO
&
posterior
muscle.
hypothprimary
active
transport
called
proton
pump
andactivity
regulation
of
acid-base
balance.`
+
3
2
H + Hb → HHb
alamus)
&
inhibitory
(midbrain)
centers.
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BASIM ZWAIN LECTURE NOTES