14. Renal Tubular Transport Flashcards
what is reabs-ed in the PCT
NaHCO3 - initatied by Na/H exhanger (85%)
NaCl - 65% total Na
K+ - via paracellular path 65%
glucose, AA - 100%
h2o - 65% total reabs passively
what is the purpose of the Na/K ATPase in the basement membrane
reabs Na into interstitum to maintain low intracell Na
what occurs in the straight segment of the proximal tubule
acid secretory system secrete organic acids into luminal fluid
(uric acid, NSAIDs, diuretics, antiobiotics)
what are carbonic anhydrase inhibitors used for
decrease H formation inside PCT
decrease Na/H antiport
increase Na & HCO3 in lumen
increase diuresis
increase urine pH (decrease body pH)
where is water reabs in the loop of henle
thin descending limb
what occurs at the thin ascending limb of LoH
almost nothing
relatively impermeable to h2o & other ions/solutes
what occurs at the thick ascending limb of LoH
25% reabs Na
(impermeable to h2o)
how is NaCl reabs-ed into interstitial space in thick ascending limb
- luminal side - Na/K/2Cl cotransporter (NKCC2) - establish ion concentration gradient in interstitium
- increase [K] in cells –> back diffusion of K into tubular lumen –>
- allow lumen-positive electrical potential to drive cation (Mg, Ca) reabs via paracellular pathways
what is reabsed at the DCT and how
10% NaCl via thiazide-senstive Na-Cl co transporter
Ca2+ -passively via Ca channels
==> results in d_ilute tubular fluid_
what do you get if you inhibit Na/K/2Cl ccotransporter
(do so w/ loop diuretics)
decrease intracel Na, K, Cl in TAL
decrease K back diffusion & positive potential
decreased reabs of Ca & Mg
increased diuresis - decrease urine pH (increases body pH)
what happens with use of thiazide diuretics
inhibit Na/Cl cotransporter (NCC)
inhibit NaCl reabs in DCT –>
increase luminal Na & Cl & increase diuresis (decrease urine pH)
How is NaCl reabs in collecting tubule
2-5% NaCl reabs thru epithelial Na channel (ENaC)
aldosterone increase expression of ENaC–>
basolateral Na/K ATPase lead to increase Na reabs & K secretion –>
retain h2o –> increase blood vol & BP
what is the most important site of K+ secretion
collecting tubule (CCT)
what do you get when a diuretic acts upstream to CCT
increase Na delivery
enhance K secretion
How is H+ secreted in the CCT
by proton pump (H-ATPase) into lumen @ alpha intercalating cells & increase urine acidity
what does ADH do at the CCT
control permeability of CCT to h2o
control expression of aquaporin-2 into apical membrane
regulated by serum osmolality and volume status
what happens with absence of ADH
impermeable to h2o –> make dilute urine
(ADH can be decreased by alc –> lead to increase urine production)
what are the two mechanisms for K sparing diuretics
- inhibit aldosterone receptor - decrease ENaC
- inhibit ENaC
==> - increase Na excretion - increase diuresis - decrease K excretion -increase urine pH
what stimulates Na reabs
- hyponatremia, low Na diet
- Na loss thru severe diarrhea
- angiotensin II
- aldosterone
what stimulates Na secretion
increased [Na] in ECF
increased tubular flow rate
what stimulates K reabs
hypokalemia (low K diet)
K loss thru severe diarrhea
what stimulates K secretion
- increased [K] ECF
- aldosterone
- increased tubular flow rate
- Na delivery to cortical CD
what is the urea permeability in inner medullary collecting duct (IMCD)
during anti-diuresis - h2o reabs in CCT
urea flows thru the duct & is concentrated in IMCD
high [urea] promotes passive reabs down [] from IMCD into interstitium
- go to LoH where [urea] is low –> flow down gradient into LoH
what does ADH do to NKCC2 channels in TAL
increase presence of NKCC2 channels – increase permeability of NaCl at apical mem of TAL
increase reabs –> increased osm
IMCD gets very concentrated bc Na & urea –> greater urine concentrating abliity
