Renal Physiology II

1
Renal Physiology II

• Urination
• Tubular Transport
• Countercurrent

2
Getting Urine from the kidney to the outside.
(Urination or micturition) Processed tubular
fluid is dumped by the collecting system into the
renal pelvis where it enters the
ureters. Ureters conduits that propel urine by
peristaltic contractions toward the
bladder. Bladder a muscular bag that holds
urine and forces it by contration. Urethra the
conduit for urine from the baldder to the
outside
3
Pelvis Collects urine from collecting ducts. In
the pelvis there are electrical pacemaker cells
that initiate peristaltic waves in the (2) smooth
muscle sheaths of the ureteral wall. (The pelvis
to ureter is a functional syncitium, not unlike
the muscular wall of the heart). The frequency of
the waves is 2-6/min. The pacemaker cells seem to
be stimulated by the stretch of urine filling the
pelvis. The movement of the peristaltic wave is
about 2-6 cm/sec., traveling from its origin at
the pelvis down to the bladder.
Urethra ?
4
Anatomy of the bladder and ureter. On the right
is the electrical profile of a peristaltic wave
passing down the muscular wall of the ureter.
Page 752
5
The peristaltic waves propel the urine along the
ureter, generating a pressure head of which
changes from a baseline of 2-5 cm H2O up to 20-80
cm H2O. While peristalysis is independent of
nerve input, the action of symapthetic nerves
innervating the ureter may modify the rate or
force of peristalsis. Interruption of the flow of
urine by an obstruction (such as a kidney stone)
stops flow, increases pressure which can back up
through the ureter into the pelvis, and increase
the nephron and subcapsular hydrostatic pressure.
This may result in the condition hydronephrosis
in which the medulla is damaged and may even be
sloughed off, leaving a hollow kidney. Obviously
this condition impares the concentrating ability
fo the kidney. There are autonomic pain fibers
in the ureter which account for the acute pain
when a kidney stone is formed.
6
The bladder and its sphincters is also innervated
with sympathetic, parasympathetic and somatic
(voluntary) nerves. The wall of the bladder is
composed of three muscular layers, called the
detrusor muscle. A triangular membrane called
the trigone acts as a valve system along with
the internal sphinctors of the muscular wall to
prevent urine reflux into the ureters.
7
Again, the anatomy of the bladder note trigone.
Page 752
8
Sympathetic nerves originate from the neurons ot
the intermediallateral cell column from T-10 to
L-2. they innervate the body of the bladder and
the trigone. Parasympathetic nerves originate
from S2-S4 of the sacral spinal cord. They
innervate the body and neck of the
bladder. Somatic innervation (voluntary or
pudendal) originates from the motor neurons
arising from S-2 to S-4. They innervate and
control the voluntary muscles of the external
sphinctor.
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Bladder tone is derived from the volume and
pressure exerted on the inside of the bladder
(intervesical pressure). Increasing bladder
volume by 50 ml increases pressure. As volume
inceases further, the intervesical pressure
increases, but not much until you get above 300
ml. then the pressure rises steeply with
additional volume. (see next slide-blue
line). This increase in volume and pressure
increases bladder tone triggering the
mictiurition reflex (open the flood-gates!) Effere
nt impulses from the brain supress the reflex (a
learned reflex) until a decision is made to relax
the external sphinctor using voluntary nerves.
Voiding begins with relaxation of the external
sphinctor, then the internal sphinctor.
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Next, the detrussor muscle of the bladder wall
contracts in waves (see red lines in previous
figure) to expell the urine. Voluntary
contraction of the abdonimal muscles further
contracts the bladder, increasing the
voiding. Once the bladder is empty, we are back
down to the no tone phase (in the lower left
corner of figure 32-14) and the sphinctors can
close again. The process is sterile until it
leaves the body. However, because of all the
organic and waste material, once out is it a good
culture media.
13
The urethara in the man passes through the
prostate gland. As the prostate enlarges, due
to age related hypertrophy or prostate cancer, it
constricts the ureter and makes voiding
difficult, despite intact bladder and sphincter
reflexes. The purpose of the prostate is to
provide urologists with a large source of income,
as well as extensive extramural research funding
and publications.
14
SECTION II Transport along the nephron
15
Transport of Sodium (Na) and Chloride (Cl-)
Chapter 34 The filtered load of Na is the
product of the glomerular filtration rate (GFR,
180 liters/day) and the plasma Na concentration
(142 mM), or approximately 25,500 mM/day
(equivalent to the Na in approximately 1.5 kg of
table salt, more than nine times the total
quantity of Na present in the body fluids. With
a typical Western diet consuming approximately
120 mM of Na per day, the kidneys reabsorb
approximately 99.6 of the filtered Na by the
time the tubule fluid reaches the renal pelvis.
Therefore, even minute variations in the
fractional reabsorptive rate could lead to
changes in total-body Na that markedly alter ECF
volume, sodium balance, blood pressure, body
weight and many other
16
The filtered load of Na is 25,500 mM/day, but the
intake is only 120 mM/day and the output is 100
mM/day excreted plus about 20 mM in the feces and
sweat. Thus, the intake equals output, so the
body is in sodium balance.
17
Reabsorption of filtered Na load along the each
nephron segment. Yellow boxes are the amount of
filtered which is reabsorbed. Green boxes
represent the amount of filtered which remains in
each portion of the nephron.
Pg 776
18

• Transport of ions, and particularly of sodium
  from the lumen to the blood across the tubular
  wall is through two pathways transcellular and
  paracellular.
• Transport is driven by two general mechanisms
• active transport in an energy (ATP) utilizing
  fashion where ions are pumped against their
  electrochemical gradient (uphill), and
• passively down their electrochemical gradient
  (downhill) along the gradients created by the
  active transport.

19
Tubular epithelial wall
Capillary wall
Start here with Na delivery
End here with sodium reabsorbed and recovered
Tubular lumen
Interstitial space
Capillary Lumen
Na
Apical Membrane
Basal-lateral membrane
Na
Na
Na
Na
Net pathway for sodium (Na) reabsorption from
tubular lumen to capillary
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Para-cellular movement incorporates The
transepithelial electrochemical Na gradient
drives passive Na reabsorption in the proximal
and thick ascending limb of the nephron. Not so
for later nephron segments where the net
(passive) force favors movement into the lumen.
Na can also move passively in the proximal
tubule (without active transport) via solvent
drag where the movement of water (driven by
active Na transport) sweeps additional Na and Cl
along with it (a sort of mass-action) out of the
lumen into the lateral intracellular space. The
leakiness of the nephron (facillitating passive
reabsorption) is greatest in the proximal, and
decreases along the nephron to the papillary
collecting ducts.
22
Trans-cellular movement incorporates 1) passive
entry from the lumen via the apical membrane
into the cell down an electro-chemical gradient.
The proximal, TAL and DCT use various
co-transporters and exchangers, while in the
collecting ducts Na enters via Na channels. 2)
Active extrusion of Na out the basal-lateral
membrane via a Na-K pump which maintains
intracellular Na low and K high. This exchange
keeps the voltage at 70 mV (cell interior
negative vs interstitium, or lumen) depending on
pump activity and the voltage gradient it
creates.
23
There is a net driving force due to the active
pump forcing Na into the interstitium, but a net
negative change favoring the lumen to draw Na
back via extracellular junctions.
Downhill refers to a passive flow along an
electrochemical gradient not requiring active
transport.
24
Proximal the Na-K pump on the apical
(interstitial side) membrane is the driving force
for the electrochemical gradient which drives
passive transport into the cell and keeps
intracellular Na low, pumping against the
gradient into the basal-lateral space. Passive
entry into the cell is by diffusion, facillitated
diffusion through a transporter or
co-transporter, and by electroneutral exchange
with hydrogen ions (H).
Na
Na
Interstitial space
Tubular lumen
pump
Na
25
Na reabsorption in different nephron segments
26
The sodium movement across the thin limbs
(decending and ascending limbs) of the loop of
Henle are virtually entirely passive down its
electrochemical gradient and paracellular. Keep
this in mind when we return to the countercurrent
system!.
27

• Thick Ascending Limb (TAL) of the loop of Henle.
• Transcellular Na reabsorption includes
• the Na/K/2Cl co-transporter (NKCC2) which couples
  inward movement of these three ions in an
  electroneutral (2 2-) process driven by the
  downhill gradient of Na and Cl into the cell.
  (Note that this pump is the target of loop
  diuretics). Much of the K entering the cell is
  extruded via K channels down its own gradient.
• The Na-H exchanger exchanging sodium for
  hydrogen in an electroneutral process.

28
Na reabsorption in different nephron segments
29
Paracellular sodium transport by the thick
ascending limb (TAL) (also known as the
diluting segment). Because the lumen of the TAL
is positive voltage due to the high density of K
channels in the apical membrane, unlike all other
nephron segment epithelia. This lumen-positive
voltage drives sodium (and other positively
charged ions) out of the lumen across the tight
junctions between the cells. This paracellular
pathway accounts for about half of the sodium
movement out of the lumen to the basalateral
spaces and the interstitium. The TAL has low
water permeability, so removal of ions without
water following leaves the lumen dilute
(hypoosmotic) and the interstitium concentrated
(hyperosmotic).
30
Transcellular and paracellular Na reabsorption in
different nephron segments
31
Distal Convoluted Tubule (DCT) Sodium
reabsorption in the distal tubule is almost
entriely due to transcellular transport. Electrone
utral passive apical Na entry is due to an Na/Cl
cotransporter (NCC). Unlike the NKCC2, this is
independent of K (this pump is the target of the
thiazide diuretics, which tqarget sodium
without wasting potassium) The net movement of
transcellular sodium in the DCT is driven by an
ATP-utilizing basal-lateral Na-K pump
32
Transcellular and paracellular Na reabsorption in
different nephron segments
33
Sodium transport in the Collecting Tubules The
relatively modest Sodium reabsorption in the
collecting tubules is entirely transcellular via
the principal cells. Na enters the apical
membrane via a voltage-gated sodium channel or
ENaC. The basolateral movement of sodium out
of the cell is driven by an energy requiring Na-K
pump which establishes the gradient driving
apical sodium entry. The movement of Na out of
the lumen into the cell makes the lumen
negatively charged, and the movement of K out of
the cell, primarily into the basolateral
interstitium makes the cell negative, for a net
transepithelial voltage of -40 mV. The hormones
aldosterone and vasopressin can change this site
of transport .
34
Transcellular and paracellular Na reabsorption in
different nephron segments
35
Medullary Collecting Duct The inner and outer
medulalry collecting ducts reabsorb only a small
amount of sodium (3 of filtered load) and this
is probably via ENaC on the apical membrane and
the Na-K pump driving Na movement on the basal
lateral membrane.
36
Cl- transport and reabsorption Most Cl follows
along with Na reabsorption, but the exact nature
fo the movement is somewhat different. In the
Proximal tubule Early proximal tubule Cl
reabsorption is mostly paracellular via solvent
drag driven by the lumen negative
potential. However, in the late proximal it is
reabsorbed by a predominantly by transcellular
pathway, driven by apical H exchange and active
transport with Na and a K cotransporter. The
lumen becomes positive actually retarding Cl
reabsorption.
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38
Changes in proximal TFP ratio along the length
of the proximal tubule. Note that 65 of the
water is lost so inulin continues to concentrate,
while osmolality and Na are unchanged.
39
Thick ascending limb (TAL) Cl is primarly
reabsorbed by the NaK2Cl co-transsporteracross
the apical membrane, and basal lateral Cl
channels along with active transport of sodium
drive Cl into the interstieium. Distal Tubule
Apical Cl reabsorption occurs via a Na/Cl
ccotransporter and is driven by Cl following Na
active extrusion via a Na/K pump. Collecting
ducts The principal cell has an electrogenic
pump that creates a -40 mV lumen negative
potential that drives Cl- out of the lumen via
paracellular routes. However, the other cell
type (the intercallated cell) drives
transcellular Cl movement powered by a
basalateral H pump.
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42
Water Reabsorption In the proximal tubule,
water follows sodium passibvely and isosmotically
because the proximal tubule is very permeable to
water. Water moves both transcellularly and
paracellularly. The transcellular movement is
facillitated by aquaporin water channels in
both the apical and basalateral membranes.
43
Water reabsorption in the Thick Ascending Limb
and Distal nephrons. All the distal nephrons,
from TAL on, have a very low water permeability
(in the presence of vasopressin). This low water
permeability will be very important in
understanding countercurrent concentration of
the urine (coming later) The combination of Na
transport with low water permeability produce a
dilute tubular fluid with low Na and low
osmolality. This facillitates later passive water
reabsorption down a concentration gradient out of
the nephron and into the capillary blood.
44
End here for now
45
Because of the high energy involved in active
reabsorption by the nephron using ATP and the
generation of ATP by oxidative metabolism, the O2
consumption by the kidney (cortex) is very high.
While the kidneys are only 0.5 of the total body
weight, they account for 7-10 of O2 consumption.
The figure shows that there is a dirct
correlation between sodium reabsorption and O2
consumption.
46

• Regulation of Na transport by glomerulotubular
  balance
• Changes in renal hemodynamics change Na load
  presented to the kidney and the glomerulotubular
  balance in the proximal tubule.
• When the Na load is changes, proximal
  reabsorption changes proportionately such that
  the amount reabsorbed is a constant fraction of
  that filtered.

Absolute reabsorption of Na (mM/min)
47
What factors regulate glomulotubular (G-T)
balance? Starling forces are altered when the
filtration fraction is changed. Normally in the
capillaries, hydrostatic pressure is low and
oncotic pressure high. This may be changed by
altering the amount of solutes and water
filtered. Thus, the changes that take place
reflect the changes in filtered load and what the
proximal must deal with. Internally the
presentation of more Na into the lumen means more
substrate to be reabsorbed. Altered filtered
load will also change the Starling forces in the
capillary and affect the net driving force for
reabsorption. Finally, certain humoral factors
(angiotensin, nitric oxide) directly affect Na
reabsorption and so can alter G-T balance
48
Humoral factors modulate glomerulotubular
balance Renin-angiotensin-aldosterone
aldosterone stimulates Na reabsorption in the
collecting tubules via ENaC channels and the
basal lateral Na-K pump. Angiotensin itself can
directly reduce Na reabsorption. Sympathetic
renal innervation release norepinephrine release
to reduce RBF, GFR, and reduce Na excretion.
Renal nerves also may stimulate renin and further
induce the renin angiotensin system. Arginine
vasopressin (ADH) from the posterior pituitary
which produces a concentrated urine and conserves
H2O. It acts by increasing the water permeability
of the collecting tubules and increasing Na
reabsorption .
49
Distal Flow-dependent reabsorption Distal sodium
reabsorption also increases with an increased
distal sodium load. Increased flow and Na
delivery increases the work load of the pumps
which can work more at higher flows. However,
this is not a linear relationship as in the
proximal, as the cululative Na reabsorption may
only increase at a ration of half that of the
increase in distal delivery.
50
NEXT SECTION Transport of other molecules Urea,
glucose, Phosphate, Calcium, magnesium and
organic solutes. Beyond sodium, chloride and
water, the kidney handles other substances which
are important in homeostasis.
51
Urea is produced primarly in the liver as a
bi-product of amino acid metabolism. The MAIN
pathway for the body to eliminate this waste
product is through the kidney. Urea is freely
filtered by the kidney, then both secreted and
reabsorbed (overall, there is net reabsorption,
so the clearance of urea is 60 less than the
GFR). Proximal tubule and medullary collecting
duct are the main sites for reabsorption. The
thin limbs of the loop of Henle are the primary
sites for secretion.
52
Urea
53
Water leaves the proximal tubular lumen dragging
urea, so reabsorption is linked to flow. However,
urea does not leave as efficiently as sodium, so
the luminal urea concentration rises, creating a
diffusion gradient out of the tubule. In the loop
of Henle, in the medullary interstitium, urea
concentration is high. The thin limbs of the loop
have a urea transporter (UT2) which secretes urea
into the lumen via facillitated diffusion.
Luminal concentration rises to 110 of the
filtered load by the end of the loop. In the
medullary collecting duct, urea is reabsorbed by
apical and basalateral facillitated transport
(UT) due to the high luminal urea concentration.
This movement into the deep medulla helps keep
interstitial urea concentration high for the
countercurrent system.
54
Glucose Transport Glucose in the blood is
tightly regulated by insulin at 4-5 mM (70-100
mg/dL). Glucose is freely filtered by the
glomerulus, by 98 of the filtered glucose is
reabsorbed by the proximal tubule. Normally,
virtually no glucose appears in the
urine. Proximal glucose transport is active
coupled to sodium transport via sodium-glucose
co-transporters (SGLT) on the apical membrane and
across the basalateral membrane by facillitated
diffusion (via GLUT 1 and 2). In the early
proximal it is driven by a high capacity, low
affinity transporter (SGLT2), but later along the
proximal by a low capacity, high affinity
transporter (SGLT1).
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While glucose is normaly totally reabsorbed, if
the plasma levels start to increase, the filtered
load will increase and it can surpass the ability
of the nephron to totally reabsorb it. This
maximum level is referred to as the transport
maximum (Tm). It reflects a point where the SGLT
transporters are totally saturated, so any
filtered glucose beyond that maximal amount
reabsorbed will begin appearing in the urine.
Coupled to the saturation of the transporters,
the clearance of glucose (which is normally zero)
will begin to rise, reflecting a fraction of the
total filtered which now appears in the urine.
See figure 35-5 on page 794
58
Glucose filtration (yellow), reabsorption (red)
and excretion (green) vary as the transport
maximum of the nephron is reached at around 250
mg/dL.
Glucose clearance is normally 0, but beyond the
capacity of the nephron to reabsorb, it starts
increasing as a percentage of the filtered load
spills over into the urine.
59
Reabsorption of Amino Acids The body does not
want to lose their nutrient substrate amino
acids, so while the kidney freely filters them,
they are normally totally reabsorbed. Apical
amino acid transport is typically active by a
sodium-dependent co-transporter, though some
amino acids are reabsorbed via Na-independent
facilitated diffusion. On the basal lateral
membrane most amino acids exit the cell by
facilitated diffusion. In some cases, due to
similar molecular structures, the amino acids may
exhibit competitive inhibition of transport.
Amino acid transport kinetics are similar to
glucose, in that they exhibit a transport maximum
and may saturate if plasma levels are too high.
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61
Reabsorption of other molecules by the
kidney. Oligopeptides filtered oligopeptides are
totally reabsorbed in the proximal
tubule. Proteins proteins (and protein
fragments) are typically not filtered, but those
that are get reabsorbed by receptor-mediated
endocytosis, metabolized and taken back into the
blood stream, so that only trace amounts show up
in the urine. Carboxylates (pyruvate and
lactate) are products of anaerobic glucose
matabolism and are sued as intermediates in the
citric acid cycle. These are totally conserved by
reabsorption by the kidney Organic anions and
cations are metabolic products secreted by the
late proximal tubule. Phosphate Similar to
calcium, 90 of filtered ionic free phosphate is
reabsorbed by the kidney, mostly in the proximal.
62
Calcium
63

• Calcium in the plasma
• The total concentration of calcium in plasma is
  normally 2.2 to 2.7 mM (8.8-10.6 mg/dl).
• Some 40 binds to plasma proteins, mainly
  albumin, and constitutes the nonfilterable
  fraction.
• The filterable portion, approximately 60 of
  total plasma calcium, consists of two moieties.
• approximately 15 of the total, complexes with
  small anions such as carbonate, citrate,
  phosphate, and sulfate.
• approximately 45 of total calcium, is the
  ionized Ca2 that one may measure with Ca2
  -sensitive electrodes or dyes. It is the
  concentration of this free, ionized calcium that
  the body tightly regulates plasma Ca2
  normally is 1.0 to 1.3 mM (4.0-5.2 mg/dl).

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The renal tubule has the ability to vary its
reabsorption of filtered calcium to adjust for
changes in intake or increased calcium
requirements. Under normal conditions, lt1 of
filtered calcium is excreted in the urine.
Calcium is reabsorbed throughout the nephron
Most of the regulation of reabsorption occurs
in the distal nephron. In the thick ascending
limb of the loop of Henle (TAL), calcium
reabsorption occurs through a primarily
paracellular pathway, but active, transcellular
reabsorption may occur as well during stimulation
with parathyroid hormone (PTH).
66
Calcium reabsorption in the PROXIMAL TUBULE. The
proximal tubule reabsorbs approximately 65 of
the filtered Ca2, a process that is not subject
to hormonal control. A small part of the Ca2
reabsorbed by the proximal tubule (20 of the
65) moves via a transcellular route. Most
proximal tubule Ca2 reabsorption (80 of the
65) occurs via the paracellular route.
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Calcium Transport in the THICK ASCENDING LIMB.
The thick ascending limb (TAL) reabsorbs
approximately 25 of the filtered Ca2. Under
normal conditions, about half of Ca2
reabsorption in the TAL occurs passively via a
paracellular route, driven by the lumen-positive
voltage. Thus, it is not surprising that
hormones such as AVP, which make the
transepithelial voltage more positive, indirectly
increase Ca2 reabsorption. The other half of
Ca2 reabsorption by the TAL occurs via the
transcellular pathway, which is stimulated by PTH
.
69
Calcium enters the apical side passively, and
most is then extruded via active transport out of
the cell into the basal lateral interstitium.
CaSR on basal-lateral surface may inhibit Ca
transport and NaKCl co-transport
70
Calcium in the DISTAL CONVOLUTED TUBULE. This
segment reabsorbs approximately 8 of the
filtered Ca2 load. Despite the relatively small
amount of Ca2 delivered, the distal convoluted
tubule (DCT) is a major regulatory site for Ca2
excretion. In contrast to the proximal tubule and
TAL, the DCT reabsorbs Ca2 predominantly via an
active, transcellular route.
71
PARATHYROID HORMONE The most important regulator
of renal Ca2 reabsorption is PTH, which
stimulates Ca2 reabsorption in the thick
ascending limb, the distal convoluted tubule, and
the connecting tubule. (PTH does NOT have a
proximal action) PTH appears to increase the open
probability of apical Ca2 channels. Such an
increase in Ca2 permeability would increase
intracellular Ca2i, which in turn would
stimulate basolateral Ca2 extrusion mechanisms,
increase Ca2 reabsorption, and raise plasma
Ca2 .
72
Calcium reabsorption in the Distal
Convoluted Tubule (DCT) Because only a small
percentage of filtered calcium is excreted in the
urine (0.5), and the DCT is the last major sight
for reabsorption of calcium, relatively small
changes in the fraction reabsorbed in the DCT
result in large changes in the total amount of
calcium lost in the urine. Reabsorption in the
DCT is regulated by PTH. When serum calcium
concentration decreases, PTH release from the
parathyroid glands increases. This effect is
mediated by the calcium-sensing receptor (CaSR)
in the parathyroid gland. PTH acts on the DCT
to increase calcium reabsorption.
73
K, Potassium
The distribution of potassium is very different
from sodium, as it is the most abundant
intracellular cation, as 98 of the bodies K
lies within cells. The circulating K is tightly
regulated at a low 3.5-5.0 mM (compared to 145 mM
for Na). K within cells is essential for
maintaining cell volume, regulating intracellular
pH, controlling enzyme function, DNA, protein
synthesis and cell growth. The ratio of
intracellular to low extracellular K is critical
in maintaining the electrical potential across
cell membrane (in both excitable and
non-excitable cells).
74
Potassium homeostasis The body must remain in
K balance, such that intake equals output.
(about 80-120 mM K/day in and out). Typically
the kidney filters 800 mM/day, so the excretory
load is about 10-15 of that filtered. K
handling and regulation by the kidney includes
the ability both to reabsorb and to secrete.
75
90 of filtered K is reabsorbed by the end of the
loop of Henle. Regulation of K balance depends
on the 5 distal nephron segments
76
Most (80) of K reabsorption takes place in the
Proximal tubule Proximal reabsorption of 80 of
the filtered load takes place by passive
paracellular movement via solvent drag and simple
diffusion, driven by the gradients established by
active sodium reabsorption. Potassium
reabsorption in the proximal (because of its
passive paracellular nature) is highly dependent
on fluid movement out of the lumen, following
sodium. The basalateral Na-K pump does NOT
directly affect K rabsorption since the movement
is mostly paracellular and not dependent on the
intracellular gradient (remember that the Ki is
high and works against transcellular K movement!)
77
K reabsorption in the thick ascending limb
accounts for an unregulated additional 10 of the
filtered load. The thin limbs of the loop of
Henle secrete K (passively) due to the high K
concentration in the medullary interstitium. The
TAL reabsorbs K by both paracellular and
transcellular pathways, Paracellular passive
reabsorption is driven by both high K
permeability and the lumen positive voltage.
Transcellular reabsorption is driven by the
NKCC2 co-transporter moving sodium and K into the
cell via the apical membrane, driven by the
active movement of Na (due to the basalateral
Na-K pump) across the cell.
78
Transcellular K
50
Paracellular 50
79
In the collecting ducts , the two cell types have
different functions The principal cells secrete
K Secretion requires a basalateral Na-K
exchanger to let K enter the cell against it
gradient, and K channels on the apical side to
allow K to flow into the lumen, down its
chemical gradient. The intercalated cells
reabsorb K Reabsorption requires an apical K
pump to push K into the cell, and K channels on
the basalateral membrane to allow K to leave the
cell down its chemical gradient.
80
K Secretion
K Reabsorption