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Tubular Resorption and Secretion (managing sodium (in tubules (distal…
Tubular Resorption and Secretion
managing sodium
epithelial transport
driving force is Na-K-ATPase
all fluid resorption is tied to Na
most important fxn of the kidney
most renal E
ECF volume is Na dependent
Na is restricted to ECF
water follows [Na]
body tonicity is tightly regulated to 'set point'
add or subtract water to achieve
Na determines volume of ECF
which determines tissue perfusion
does not
determine [plasma Na] usually
[plasma sodium] = Na/H20
total body sodium = Na in grams
vast majority of Na is reabsorbed
in tubules
PCT - isotonic
distal tubule and collecting duct
early DCT - impermeable to water
site of regulation
aldosterone
Na resorption is "load-dependent"
Na transport mechanisms differ by location
early distal tubule
Na
Cl
late distal tubule and CD
Na
K
only about 3% of filtered Na reabsorbed
fine adjustments to Na excretion occur here
cell types
principal cells
Na reabsoption
K secretion
water resorption
Na channels rather than transporters
moved down e- chemical gradient
accomoanying anion is Cl-, which reamins in tubule
alpha-intercalated ells
K reabsorption
H secretion
influence by acid-base status
aldosterone
insertion of Na channels
in Loop of Henle
[Na] higher as loop descends
thin ascending limb
Na pumped out
permeable to NaCl
impermeable to water
doesn't do anything active
thin descending limb
permeable to water and small solutes
Na and urea permeable
brings fluid out
reduce amount of fluid in tubule
also doesn't do anthing active
thick ascending limb
active resorption of Na
load dependent
impermeable to water
active cells here
more diluted fluid
allows body to make both concentrated and diluted urine
proximal tubular Na reabsorption
there were stars around this so you might wanna care
early PT
picks up important stuff
reabsorbed with HCO3 and organic solutes
apical transport
Na down gradient
anions move against their concentration gradient
uses E from Na transport to reduce E cost
Na-nutrient and phosphate tsymporters
Na-H aniporters
lumen negative potential due to Na-glucose and Na-AA transport
Na draws important stuff with it
most Na resorption is by Na-H transporter
carbonic anhydrase
bicarbonate production
late pT
reabsorbed with Cl, no organic solutes
midpoint PT
100% reabsorbed by now
glucose
amino acids
lactate
85% filtered HCO3 reabsorbed
most filtered phosphate reabsorbed
large portion of NA reabsorbed
anion concentrations will be variable at this point
late proximal tubule
entering fluid very different from glomerular filtrate
most organic solutes gone
high in Cl-
HCO3 was preferentially absorbed earlier
most water removed by now
primarily reabsorption of NaCl
driven by high Cl-
transcellular and paracellular components
isometric reabsorption in PT
Na enters cells, water follows
Na pumped out by NaK-ATPase, water follows
isomsomotic fluid drawn into capillaries by Starling forces
resorption rate is dependent on amount of solute presented to tubule
the basics
reabsorbed in most segments
driven by Na-K-ATPase (active)
most isosmotic - water follows
from loop of henle on, [salt] is greater than water
different methods of reabsorption in different tubule segments
goal is
effective circulating volume
all tissues adequately perfued
sensors
baroreceptors in carotid sinus and aortic arch measure BP
volume receptors in atria
juxtaglomerular apparatus to measure renal perfusion
signals and targets
synapthetic n. output
afferent arteriole
proximal tubules
atriopeptin/atrial natriuretic peptide (ANP)
efferent arteriole
collecting tubules
renin-angiotensin-aldosterone system
proximal tubules
collecting ducts
pre- and post-glomerular arterioles
target is sodium
glomerotubular balance
constant fraction of the filtered load of the nephron is reabsorbed across a range of GFRs
if GFR increases, water and solute resorption increases
regulation of tubular Na resorption is more important than control of GFR
changes in GFR = proportional changes in reabsorption of NA in prx. tubes.
% of filtered Na remains constant
proportional amount of tubular fluid is recaptured in the peritubular capillaries due to oncotic pressure
mechanisms
preventing excessive urainary Na loss
autoregulation
is first line of defense against loss though
GT balance depends on relationship between...
filtration fraction
peritubular starling forces
oncotic pressure determines how much fluid will be kept in lumen
dehydrated = increase resorption
too hydrated = decrease resorption
managing potassium
principal intracellular ion (98% in cells)
constantly being pumped back into cell
movement as little as 2% into ECF could be fatal
infleuncing factors
physiologic
Na-K-ATPase
catecholamines
insulin
[plasma K]
exercise
pathologic
extracellular pH
hyperosmolarity
rate of cell breakdown
chronic disease
kidenys is major route of K excretion
freely filtered
almost all is reabsorbed
primary event is secretion of K into distal tubule
principal cells
cortical ad outer medullary collecting tubule
in state of K depletion, net distal reabsorption may occur over secretion
managing phosphorus
must be unbound to go through filter
freely filtered
reabsorbed in PT
saturable Tm
FGF-23 and PTH regulate reabsorption by lowering Tm
inhibits cotransporter
increases excretion
FGF-23
progressive release with increased P load
inhibits absorption of tubular P
PTH
activated if P continues to increase,
activated when calcitriol decreases
GFR is primary factor influencing retention
usually protein bound inplasma
managing calcium
must be unbound
free filtered
reabsorbed in
PAL and PT
passive and paracellular
electrochemical driving F dependent on Na reabsorption
DT
site of PTH endocrine control
only segment where reabsorption isn't linked to Na
partially protein bound in plasma