Tubular Reabsorption & Secretion Flashcards
steps of solute/water reabsorption
tubule –> interstitium –> capillaries
is reabsorption the same across the entire nephron
no - spatial; different components get reabsorbed at different points along the tubule
types of transport
paracellular (between cells)
transcellular (through cells)
what does it mean that transporter mediated transport is saturable?
reabsorption is dependent on the number of available transporters - will reach a maximum rate when all transporters occupied
is filtration saturable
NO - filtration only depends on GFR and plasma concentration
what does it mean if there is no solute detected in the urine
filtration of solute = reabsorption of solute
does reabsorption increase with filtration
yes - reabsorption and filtration will increase at the same rate until plasma concentration of the solute gets too high and all transporters are occupied (causes filtration to continue increasing while reabsorption plateaus)
what does reabsorption depend on
plasma concentration
GFR
Tm
what is transport maximum (Tm)
the maximum rate of reabsorption (mass of solute that can be transported per minute)
appears as a constant Y value (horizontal line)
what is renal threshold
the plasma concentration of a substance at which it begins to appear in urine (when reabsorption < filtration)
appears as a constant X value (vertical line)
how does decreasing GFR affect Tm and renal threshold
- NO EFFECT on Tm
- increases renal threshold (more time available to clear transporters)
what are the starling forces entering peritubular capillaries
efferent arterioles: low hydrostatic and high oncotic –> favors reabsorption
peritubular cap: high hydrostatic pressure of interstitium and oncotic pressure of capillaries; low hydrostatic pressure of capillaries and oncotic pressure of interstitium
what transport mechanisms are in the proximal convoluted tubule
Na/K ATPase
Na/Glu cotransporter
Na/H antiporter
Na/PO4 cotransporter
Paracellular Cl, Ca, Mg
Urea transporters
Aquaporins
what is the osmolarity of filtrate going through the PCT
isotonic - equal amounts of solute and water reabsorbed
what transport mechanisms are in the descending loop of henle
Aquaporins
Urea transporters - secretes urea INTO filtrate from interstitium
IMPERMEABLE to NaCl
what is the osmolarity of the filtrate going through the descending loop
osmolarity INCREASES down descending loop
urea concentration INCREASES down descending loop
what transport mechanisms are in the ascending loop of henle
Na/K ATPase
NKCC (Na/K/2Cl) cotransporter
Paracellular Ca, Mg
IMPERMEABLE to water
what is the osmolarity of the filtrate as it goes through the ascending loop
osmolarity DECREASES up ascending loop
what transport mechanisms are in the distal convoluted tubule
Na/K ATPase
TRPV5 (Ca from lumen –> cytosol)
NCX1 (Ca reabsorption)
Early DCT:
- NCC (Na/Cl cotransporter)
- ROMK (K excretion)
Late DCT:
- ENaC (Na transporter)
- ROMK (K excretion)
- some NCC
what is the osmolarity of the filtrate going through the DCT
hypo-osmotic filtrate enters but DCT is load sensitive
if filtrate Na concentration is HIGH - will increase reabsorption
if filtrate Na concentration is LOW - will decrease reabsorption
what transport mechanisms are used in the collecting ducts
Na/K ATPase
ENaC
ROMK
Urea transporters (ADH dependent) - reabsorbs out of filtrate ONLY when ADH is present
is reabsorption rate constant regardless of changes in GFR
NO - reabsorption rate changes with GFR to prevent excess losses
dependent on starling forces in peritubular capillaries
antidiuretic hormone action
ADH responds to high NaCl or low BP
produced in hypothalamus and secreted by pituitary
causes translocation of aquaporins and urea transporters to CD membrane
effect: increases water and urea reabsorption
how does ADH secretion vary based on hydration state
dehydrated: increase ADH
hydrated: decrease ADH
how does urea contribute to medullary hyperosmolarity
urea concentration in the filtrate increases from PCT –> DCT
when ADH is present: urea gets reabsorbed which decreases osmolarity of the tubule, leading to increased water reabsorption
what is countercurrent multiplication
creates and maintains medullary interstitial osmotic gradient
descending LoH: interstitium is hyperosmotic –> pulls water out of filtrate –> causes filtrate osmolarity to increase down descending loop
ascending LoH: hyperosmotic filtrate causes NaCl reabsorption into interstitium –> decreases filtrate osmolarity as it enters DCT
effect of differences in Na and water concentration get multiplied as fluid moves counter currently
RAAS signal
low NaCl and low BP/ECFV
sensed by baroreceptors, macula densa cells, and sympathetic nervous system
RAAS mechanism of action
sensors signal to JG cells –> increase renin secretion
renin cleaves angiotensinogen –> ANG I
ACE cleaves ANG I –> ANG II
ANG II –> binds to AT1 receptors on targets
angiotensin II targets
- efferent > afferent arterioles
- Na/K ATPase
- NCC transporter
- ROMK transporter
- adrenal gland
angiotensin II effects
- vasoconstriction (dec. RBF/GFR/P(GC)/NFP)
- increased Na reabsorption
- increased aldosterone secretion
aldosterone targets
- NCC
- ENaC
- ROMK
aldosterone effects
- increase Na reabsorption
- increase K excretion
what is the main nephron region targeted by aldosterone
collecting ducts
what are the different cell types in collecting ducts and why are there different types?
principal cells, intercalated cells
different types allow for separate regulation of Na reabsorption and K excretion / acid/base balance
principal cells
Na and K regulation
intercalated cells
H+ secretion and acid/base balance
where is the main nephron region of PO4 reabsorption
proximal convoluted tubule
Na/PO4 cotransporter
(driven by Na/K ATPase)
what stimulates PO4 reabsorption
calcitriol
low dietary PO4
what inhibits PO4 reabsorption
PTH
FGF-23
high dietary PO4
where is the main site of Ca reabsorption
proximal convoluted tubule
paracellular transport - regulated by CaSR/claudins and driven by electrical gradients
what stimulates Ca reabsorption
PTH
calcitriol
hypocalcemia
thiazide diuretics
what inhibits Ca reabsorption
hypercalcemia
furosemide
where is the main site of Mg reabsorption
thick ascending LoH
paracellular - regulated by CaSR/claudins and driven by electrochemical gradients from NKCC2
