QUESTIONS

1. Lowering extracellular K+ has what effect on nerve cell excitability?
    
2. What effect does epinephrine have on K+ distribution & why might its effect be helpful & good?
    
3. What effect does acidosis have on K+ distribution?
    
4. By the end of the proximal tubule, what has happened to filtrate K+ concentration?
    
5. Okay, so much for the proximal tubule. Now we reach the loop of Henle.  What happens to K+ here?
    
6. So much for the loop of Henle, what happens to K+ in the ascending loop?
    
7. Fine.  Fine.  So now we�re coming to the cortical collecting ducts & distal tubule.  Now what�s happening to K+?
    
8. How does aldosterone fit into this picture?
    
9. What is �potassium adaptation?�
    
10. Under what circumstances might an increase in sodium excretion go with an increase in K+ excretion?
     
11. Aldosterone (called the single most important factor in controlling Na+ resorption) controls Na+ resorption in the distal tubule & collecting duct. Since >90% of Na+ has already been resorbed by this point, this leaves only about 2% being controlled by aldosterone.  How is it then that aldosterone can be so important?
    
    
    
    
     

ANSWERS

1. Remember that K+ is tightly regulated to preserve the proper intra to extracellular ratio so that nerve conduction can be normal.  Increasing K+ extracellularly lowers membrane potential & increases excitability.  Decreased K+ extracellularly raises membrane potential & decreases excitability.
   
   
   
   
    
2. Epinephrine drives K+ intracellular esp. in muscle & liver tissue (this action being mediated by beta receptors).  When one is fighting or flighting, K+ is flinging out of muscle cells (as well as any cells suffering damage be they muscle cells or not).  Epinephrine helps put the potassium back.
   
   
   
   
    
3. Acidosis is associated with K+ moving out of the cells. Alkylosis moves in back in.  (Consider it a H+/K+ exchange). Alkalosis also increased K+ secretion, too.
   
   Respiratory acidosis (& some metabolic acidosis) will cause K+ retention at first (<24 hours) but ultimately there will be K+ secretion. We aren�t sure why this is.
   
   
   
   
    
4. As water is reabsorbed, a concentration gradient is set up favoring K+ diffusion to the interstitium & peritubular capillaries.  By the end of the proximal tubule, 50% of K+ has been reabsorbed.
   
   
   
   
    
5. K+ is secreted passively in the loop of Henle.
   
   
   
   
    
6. In the ascending loop the plot thickens.  Passive resorption occurs.  In short-looped nephrons, only 10% of filtered K+ is left.  We aren�t sure how much is left in the long-looped nephrons.
   
   
   
   
    
7. These areas can either do secretion or resorption.  Secretion is by active transport from the interstitium into the cell.  The luminal membrane is much more K+ permeable than the membrane on the outside (the basolateral membrane), so K+ tends to diffuse into the nephron.  There IS an electrostatic gradient that tends to keep K+ inside the cell but it is overwhelmed by the concentration gradient. 
   
   Resorption is by a luminal membrane pump which is slow but always on. 
   
   In the medullary collecting ducts there is resorption of K+.  K+ was secreted into the descending loop of Henle thus K+ is recycled the same way urea was recycled.
   
   
   
   
    
8. Aldosterone stimulates the Na+/K+ pump of the basolateral membrane.  It also increases K+ permeability on the luminal side.  Get what�s going on? There�s a bunch of K+ in the nephron.  Aldo wants you to dump K+ in urine & keep Na+.  It steps up the Na+/K+ pump towards the outside.  K+ is coming in & Na+ is going out to the circulation.  By increasing K+ permeability on the luminal side, K+ goes on out into the urine.
   
   
   
   
    
9. If K+ ingestion remains high for several days, the distal nephron has a marked increases in its ability to secrete K+.  This means that there is an increase in the number of pump sites on the basolateral membrane.  Aldosterone is partly responsible for this, too.
   
   
   
   
    
10. When eating a high sodium diet or having saline diuresis or osmotic diuresis or diuretics that act on the prox. tubule or loop of Henle, K+ will be lost with Na+.
    
    
    
    
     
11. Because of the huge volume of glomerular filtrate, 2% of the Na+ = 522 mmol/day.  This translates into about 30 grams of NaCl!!  Aldo can thus adjust over a wide range of sodium amount being excreted.