ulikedaggers

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We haven't covered this directly yet so I have no clue how it works. I just saw it in FC and figured it would be an opportunity for review for you MS2s.

How does a physiologic level of insulin cause both potassium influx (via Na-K ATPase) and sodium retention in kidneys simultaneously?
 
Jun 11, 2012
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We haven't covered this directly yet so I have no clue how it works. I just saw it in FC and figured it would be an opportunity for review for you MS2s.

How does a physiologic level of insulin cause both potassium influx (via Na-K ATPase) and sodium retention in kidneys simultaneously?
Insulin actively engages the Na/K AtPase pumps to enhance increased uptake of Na dependent Glucose. The uptake of Na and glucose together is known as co transporting and is the primary mechanism of glucose uptake via the GLUT transporters. Use of this mechanism is an indirect application of the Na/K. Since Na is constantly entering due to insulin (via co transporter) you need it to come from somewhere-renal reabsorption. This is via your medullary collecting ducts (similar to ADH/aldosterone- wherever the Na reabsorption is- haven't looked at it in a while). similarly potassium influx is due to its activation and used for INTRACELLULAR via Na/K influx mechanisms to counteract all that Na entering the cell. The Na/K transporter depletes serum K. The mechanism is beyond the scope of USMLE.

This is a stupid fact that FC likes to include because its a bunch of med students who create it. It is not essential to your knowledge. It is more important to know the facts above and apply them to questions that may ask you why the potassium is reabsorbed and why na is reabsorbed by the kidney.
 

GrabSlamBoot

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I think he is referring to the insulin activating the Na/K pump which pushes sodium out but at the same time will increase the gradient for sodium co transporters like SGLT-1 (used in oral rehydration therapy) so sodium can flow in resulting in increased cellular retention of sodium
 

SOML

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Insulin actively engages the Na/K AtPase pumps to enhance increased uptake of Na dependent Glucose. The uptake of Na and glucose together is known as co transporting and is the primary mechanism of glucose uptake via the GLUT transporters. Use of this mechanism is an indirect application of the Na/K. Since Na is constantly entering due to insulin (via co transporter) you need it to come from somewhere-renal reabsorption. This is via your medullary collecting ducts (similar to ADH/aldosterone- wherever the Na reabsorption is- haven't looked at it in a while). similarly potassium influx is due to its activation and used for INTRACELLULAR via Na/K influx mechanisms to counteract all that Na entering the cell. The Na/K transporter depletes serum K. The mechanism is beyond the scope of USMLE.
This (except maybe for that last part). In addition to Insulin facilitating GLUT tran's, it also shifts K+ into cells (after ingestion of K+ in a meal).

This is probably accomplished by: (following is from Guyton, 11th ed.)

"triggering of local tyrosine kinase receptors, triggering Insulin-receptor substrates by insulin.
Different types of IRS (e.g. IRS-1, IRS-2, IRS-3) are expressed in different tissues. The net effect of insulin binding include..

#2 - cell membrane becomes more permeable to many of the amino acids, potassium ions, and phosphate ions, causing increased transport of these substances into the cell".

How does a physiologic level of insulin cause both potassium influx (via Na-K ATPase) and sodium retention in kidneys simultaneously?
OP: Maybe the K+ influx isn't through Na/K ATPase, but the mechanism above...
 
Last edited:
Jun 11, 2012
341
46
Status
Medical Student
This (except maybe for that last part). In addition to Insulin facilitating GLUT tran's, it also shifts K+ into cells (after ingestion of K+ in a meal).

This is probably accomplished by: (following is from Guyton, 11th ed.)

"triggering of local tyrosine kinase receptors, triggering Insulin-receptor substrates by insulin.
Different types of IRS (e.g. IRS-1, IRS-2, IRS-3) are expressed in different tissues. The net effect of insulin binding include..

#2 - cell membrane becomes more permeable to many of the amino acids, potassium ions, and phosphate ions, causing increased transport of these substances into the cell".



OP: Maybe the K+ influx isn't through Na/K ATPase, but the mechanism above...

I have to politely disagree
I haven't taken USMLE yet but I know my shiz :)

http://ajpendo.physiology.org/content/295/3/E553

http://ajpendo.physiology.org/content/295/3/E727

http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/pancreas/insulin_phys.html

relevant material to read:
Other Notable Effects of Insulin
In addition to insulin's effect on entry of glucose into cells, it also stimulates the uptake of amino acids, again contributing to its overall anabolic effect. When insulin levels are low, as in the fasting state, the balance is pushed toward intracellular protein degradation.

Insulin also increases the permiability of many cells to potassium, magnesium and phosphate ions. The effect on potassium is clinically important. Insulin activates sodium-potassium ATPases in many cells, causing a flux of potassium into cells. Under certain circumstances, injection of insulin can kill patients because of its ability to acutely suppress plasma potassium concentrations.
 
Jun 11, 2012
341
46
Status
Medical Student
This (except maybe for that last part). In addition to Insulin facilitating GLUT tran's, it also shifts K+ into cells (after ingestion of K+ in a meal).

This is probably accomplished by: (following is from Guyton, 11th ed.)

"triggering of local tyrosine kinase receptors, triggering Insulin-receptor substrates by insulin.
Different types of IRS (e.g. IRS-1, IRS-2, IRS-3) are expressed in different tissues. The net effect of insulin binding include..

#2 - cell membrane becomes more permeable to many of the amino acids, potassium ions, and phosphate ions, causing increased transport of these substances into the cell".



OP: Maybe the K+ influx isn't through Na/K ATPase, but the mechanism above...
Guyton is correct (obviously; its the gold standard) but it doesn't clarify something important. The facilitation described is not as powerful as the Na/K ATPases. How do I know? because skeletal muscle is the most powerful tool to control glucose levels in the body for anything it can get its grubby hands on including sugar and potassium. Na/K ATPases are in abundance in all cells.
 

SOML

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I assume you're referring to my assertion about the Na/K ATPase not being the mechanism for K+ influx, if so, noted.