QUESTIONS

1. Is there tubular secretion of sodium?
    
2. Sodium enteres the proximal tubular cell from the lumen of the nephron by facilitated diffusion.  Exactly what does �facilitated diffusion�  involve?
    
3. How is Chloride resorption coupled to Sodium resorption?
    
4. What area of the nephron is the site of greatest sodium & water resorption?
    
5. At the end of the prox. tubule, what is the osmolarity of the tubular fluid like relative to plasma?
    
6. How does an osmotic diuretic cause diuresis?
    
7. What are the three most osmotically active solutes in the plasma?
    
8. Does the descending loop of Henle reabsorb sodium?
    
9. What is the osmolarity (relative to plasma) of the tubular fluid like entering the distal tubule after the loop of Henle?
    
10. What is the normal osmolarity of plasma?
     
11. Osmolarity of the tubular fluid in the late distal tubule & collecting ducts is controlled by the water permeability of the luminal membrane.  Guess what.  Your body can control/change the water permeability of these membranes to suit its needs.  How is this accomplished?
     
12. What local feedback turns ADH�s action off?
     
13. Where is the concentrating segment of the nephron?
     
14. Why did God make vasa recta?
     
15. Under what circumstances would urine SPGR be high & urine osmolarity be low?
    
    
    
    
     

ANSWERS

1. Hell no.  After sodium is freely filtered by the glomerulus, the rest of the nephron is busy trying to reabsorb it.  >99% sodium is reabsorbed & most of the kidney�s energy is spent on the reabsorption of sodium.
   
   
   
   
    
2. The facilitation involves electrostatic attraction.  The inside of the cell is mostly negative so sodium (being positive) is attracted in plus there is a concentration gradient favoring sodium going in (there�s almost no sodium inside because of sodium/potassium pump action on the other side of the cell).  Sodium may enter the cell alone or it may cotransport glucose, amino acids, chloride etc.  Remember, where sodium goes, water wants to follow.  How much water gets to follow is determined by the water permeability of that area of the nephron.
   
   
   
   
    
3. Mechanism #1:  As sodium leaves the prox. tubule, water goes, too.  (The prox. tubule is extremely water permeable).  As water leaves the tubule lumen, the concentration of chloride goes up & soon there is a concentration gradient favoring diffusion of  chloride out.  (Note, it takes a while to establish this gradient, so chloride diffusion is happening lower in the prox. tubule rather than higher up.)
   
   Mechanism #2:  The tubular lumen is negatively charged relative to the interstitial fluid (exc. around the ascending thick loop of Henle & the lower prox. tubule).  This is because, all of the sodium resorption has left the lumen depleted of positive charge.  All this negativity in  the lumen electrostatically repells the chloride out towards the interstitial fluid.
   
   Note:  in the thick ascending loop of Henle, Na+ transport is active (none of this facilitated diffusion stuff) & is coupled to Cl- transport.
   
   
   
   
    
4. The prox. tubule!  65% of total filtered Na+ & water is resorbed here. 
   
   
   
   
    
5. Since the cells here are so water permeable, Na+ & water are resorbed equally so that the tubular fluid at the end of the prox. tubule is iso-osmotic with the plasma. 
   
   
   
   
    
6. An osmotic diuretic contributes so much osmolarity to the tubular fluid that water reabsorption is disrupted.  (I�d always had this fantasy that water was some how pulled into the tubule but NOOoo!  Water isn�t added, it just isn�t resorbed.)
   
   
   
   
    
7. The three most osmotically active solutes are: Na+, Cl-, & bicarb (proteins like albumen don�t even come close - they contribute oncotically which is a totally different ball game.)
   
   
   
   
    
8. No.  It is the ascending loop of Henle that is doing sodium reabsorption in the loop.
   
   
   
   
    
9. They don�t call the Ascending loop of Henle the dilution segment for nothing.  The tubular fluid is very hypo-osmolar.  This is because the ascending loop is fairly impermeable to water.  Sodium & chloride are resorbed by the loop leaving lots of water with not too much stuff floating around in it.  The distal tubule is even less water permeable so by the time your entering collecting ducts you have some seriously hypo-osmolar urine.
   
   
   
   
    
10. 300 mosmol/L.
    
    
    
    
     
11. Easy.  This is what ADH is for.  Without ADH, water permeability is low so urine stays hypo-osmolar.  With ADH, water permeability is high so osmolarity can increase.  What a concept!  And of course there are varying degrees of ADH presence, too.
    
    
    
    
     
12. ADH induces intramedullary synthesis & release of prostaglandins which interefere with ADH-induced  generation of cyclic AMP.  (ADH works through creating cyclic AMP)
    
    
    
    
     
13. The medullary collecting ducts are the concentrating segments.  Confused?  Did you think it was the ascending loop of Henle because you vaguely remember something called �Counter current multiplication� & it had to do with concentration & the loop of Henle?  Here�s the true story:  Because the descending loop of Henle is water permeable & the ascending loop isn�t, you set up a tremendous osmolarity gradient with the tip of the loop having the highest osmolarity & the top of each limb being hypo-osmolar.  Because of the opposite directions of fluid flow in each limb of the loop, this is called �counter-current� multiplication but urine concentration doesn�t occur here.  The collecting ducts run parallel with the loops through this concentration gradient.  In areas where the duct passes through a really hyperosmolar area, water in the tubule is banging on the walls of the tubule trying to get out!!  How much water actually escapes depends on how much ADH is around.
    
    
    
    
     
14. Vasa recta are medullary vessels which run paralled to the loops of Henle & collecting ducts.  These vessels actually have hairpin turns in them so that osmolarity inside them matches the osmolarity of the loop at the same level.  If God had used normal capillaries without hairpin turns, there would be 300 mosmol/L of osmolarity inside them & the concentration gradient would equilibrate & be ruined.  All that countercurrent multiplication would be for nothing.
    
    
    
    
     
15. SPGR is really a measure of density, not concentration.  Thankfully, density correlates well with concentration.  If you had an unconcentrated urine with lots of protien in it, its SPGR would be high but its osmolarity would be low.