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Pulmonary and Renal Physiology > Tubular Transport > Flashcards

Flashcards in Tubular Transport Deck (47):

Filtered Load

FLx= Px * GFR

Plasma Concentration times GFR


Excretion Rate

UEx = Ux * V

Urinary excretion rate is urine concentration times flow


Reabsorption rate

RRx= FLx - UEx

Filtered load minus urinary excretion


Secretion Rate

RSx = UEx - FLx


Fractional Excretion

FEx = UEx/FLx


Sodium reabsorption in the early proximal tubule

Passed through apical membrane via sodium cotransporters (glucose, phosphate, etc.). Pumped out of epithelial cell at basolateral membrane via Na/K ATPase. This creates negative potential at apical side. Counter ion is bicarbonate.


How is Cl handled in the early proximal tubule?

It remains trapped. Doubles down the length of the proximal tubule.


Sodium reabsorption in late proximal tubule

Two methods 1) Trancellularly via Na-H antiporter. 2) Paracellularly via Cl-driven Na reabsorption.

1) Na pumped in, H pumped out. Simultaneously, Cl pumped in, formate pumped out. H combines with formate and diffuses in. At BL side, Na/K ATPase, Cl/K cotransporter.

2) Cl passes paracellularly, which creates a driving force (+4mV at apical side) for cationic movement. Na is the most abundant cation.


How is HCO3 reabsorbed in the proximal tubule?

No transporter at apical side! Must be converted.

HCO3 in lumen combines with H's being pumped out against Na, and via proton pumps. Forms H2CO3. Turns into CO2 and H2O via carbonic anhydrase. Diffuse in, undergo reverse reaction. H+ pumped out to apical side, HCO3 antiported with Cl at Bl side, and 3 HCO3 cotransported with Na.


Where and how is glucose reabsorbed?

100% reabsorbed in proximal tubule. SGLUT (Na cotransport) at apical side. GLUT 1 and GLUT 2 at BL side.


How is aberrantly filtered protein reabsorbed?

Proteins are degraded in the lumen. Peptides and single AAs are endocytosed, other AAs are cotransported in with Na.


How is potassium reabsorbed in the proximal tubule?

Solvent drag.


How is urea reabsorbed in the proximal tubule?

Will diffuse passively down its concentration gradient.


How is water reabsorbed in the proximal tubule?

Diffuses through membrane with CO2.


How is calcium reabsorbed in the proximal tubule?

80% paracellular, 20% transcellular via channels.


How is NH3/NH4 reabsorbed in the proximal tubule?

Absorbed via Na antiporter.


G-T Balance

Proximal tubule reabsorbs 2/3 filtrate regardless of the GFR. If GFR increases, then proximal tubule reabsorbed goes up and vice versa.


Tonicity of the fluid at the end of the proximal tubule?



Function of the Loop of Henle

Sets up concentration potential. Delivers and generates hypotonic tubular fluid. Takes salt out and makes urine more dilute. Creates a driving force for H2O out of the collecting duct.


Think descending limb osmolarity?



Thin descending limb function

Pump salt in, pump water out. This generates hyperosmotic solution inside the lumen.


Thin ascending limb function

Salt permeable, water impermeable. Some salt leaks out down gradient. Fluid becomes less hypertonic.


Thick ascending limb function

Impermeable to H2O, high degree of active salt transport out of lumen into interstitium. Hypotonic solution generated using Na, K, 2Cl transporter.


What is the relationship between Na and K transport in the thick ascending limb?

Na is 40x more abundant than K. So K is limiting factor in the Na K 2Cl active transporter. Thus, K must filter back into the loop of henle via a back leak channel. This transporter is also electrogenic as a result. So lumen is +7mV.


Is there paracellular transport in the TAL?

Yes, of cations moving with the electrochemical gradient.


How is NH4 transported in the TAL?

Sometimes will substitute for K on the transporter, but cannot back-leak.


Role of the vasa recta?

To maintain corticomedullary gradient. Will transport salt down and water up. End fluid is slightly hypertonic.


What creates such a high gradient at the loop of henle?

The activity of the Na K 2Cl transporter. This is regulated by ADH.


Role of ADH at loop of henle?

Increases activity of the Na, K, 2Cl transporter to create higher corticomedullary gradient, increases permeability of collecting duct so urea can move out, and MOST IMPORTANTLY, increases water permeability in principal cells in late distal tubule that cause water to move out of the lumen into the interstitium.


Free water

Hypotonic water. Any H2O that is not associated with an osmotic particle. TAL is first place of free water.


Free Water Clearance Equation

CH2O = V - Cosm

Where Cosm = UosmV/Posm

+=excreting free h20
-=retaining free h20


Function of the early distal tubule

Take hypotonic solution and make even MORE hypotonic. Remains impermeant to luminal H2O, Na-Cl cotransporter.


Function of the late distal tubule and collecting duct?

Reabsorb Na, Secrete K, Reabsorb Cl, Reabsorb H2O. Uses Principal Cells and Intercalated cells.


Which cell responds to aldosterone?

Principal Cell


Function of alpha and beta intercalated cells?

Alpha- secrete H, reabsorb some K
B- Secrete HCO3


What determines how much K is reabsorbed or secreted?

Balance of activity of alpha intercalated and principal cells.


Three ways the LD/CCD regulates acid base status

1) Alpha intercalated cells reabsorb HCO3. 2) Pump out H ions as titratable acid (by associated with PO4) 3) By excreting NH4.


How does the alpha intercalated cell control excretion of NH4?

Will turn glutamine into glutamate and NH4, NH3 diffuses out, protonated to NH4.


What determines what acid pathway is taken?

The amount of bicarb filtered, acid status of the blood.


Function of ADH

Retain water, has vasopressive actions too.


Where is ADH synthesized and stored? How is it made?

Supraoptic nucleus, paraventricular nucleus. Created from Pre-pro-pressophysin. Cleaved to pressophysin, cleaved to ADH.


What are the stimuli for ADH release?

Osmoreception (increases in osmolarity of 1% cause ADH release). Baroreception (decrease in volume of 10% causes ADH release).


Vascular functions of ADH

V1 mediated, causes vasoconstriction w/Gq.


Tubular functions of ADH

V2 mediated (Gs). Increase function of transporter, increase CCD permeability of urea, increased aquaporin insertion in principal cells, moving H2O out of lumen.


What causes renin release?

Decreased renal VP, decreased salt delivery to macula densa cells. = Renin increase.


Where does Ang II assert its effect? Where does aldosterone assert its effect?

Proximal Tubule, distal tubule.

Both reabsorb Na, secrete K, causing H2O retention.


Effect of ANP?

Salt and water excretion, washes out longitudinal gradient, less water movement out of CCD.