Renal Regulation of ECF K+ Flashcards
What is the relationship between insulin and K?
K regulates serum insulin.
such that if you give K, insulin goes up.
in the other direction, if you give insulin, serum K will go DOWN (bc trying to regulate it)
What is the role of catecholamines and the Beta2 adrenergic receptor (B2AR)?
Catecholamines are upregulated when you have to slam on the breaks in your car really quick and fight or flight activities like that. They bind at the B2AR and have a similar effect on K as insulin does.
as inc. insulin (or B2AR) K decreases.
insulin and catecholamines are part of the _______ (internal/external) balance on K?
internal
external has to do with what happens in the nephron and with what you eat and drink.
The major regulator of external K balance is ______ at ___% and second is the _____ at ____%.
kidney-85%
GI- 15%
What happens to K as it passes through each of the following phases of the nephron?
- glomerulus
- PCT
- LoH descending limb
- LoH ascending limb
- cortical collecting tubule (CCT)
- between late CCT and urine
- about 100% is filtered
- 50% reabsorbed
- K is added at DL so that at the hairpin turn 100% of K is present again.
- K is reabsorbed again so that when reach DCT essentially 0% of K remains.
- K added again
- about 50% of K is reabsorbed again (this is the K that will get added to the next load of K at the DL of LoH).
this is likely done to help regulate Na.
What is probably the most important location of the K secretion in the tubules clinically and why?
The CCT. These are the distal fine tuning segments following the reabsorption that occurs in the DCT.
In this location K is secreted variably to achieve homeostasis. K is actually reabsorbed and filtered many times throughout the tubules. By the time it gets to the fine tuning segments there is only a little left which is reabsorbed in the principal cells. All of the filtered potassium is obligatorily reabsorbed (meaning that it is not regulated); hence regulated potassium secretion in the fine tuning segments pretty much determines potassium excretion and ECF potassium balance.
Diseases of K, are thus referring to diseases of the CCT.
Describe the transporter mechanism and characteristics in the PCT cell.
polarized cell. connected by tight junctions. Major determinant of K reabsorption here is bulk flow or diffusion which is regulated by Na reabsorption through the paracellular space (inbetween the cells).
This is passive (follows Na) and is not regulated (so they are rarely abnormal) and thus it is not that important for us clinically and likely not for the test either.
Describe the transporter mechanism and characteristics in the AL of LoH.
There is a Na/K/2Cl transporter on the apical membrane and a Na/K/ATPase transporter on the basolateral membrane.
Na is reabsorbed with K on the apical side through the Na/K/2Cl transporter. Then through the Na/K/ATPase transporter, Na is kicked out of the cell and more K is brought into the cell on the basolateral side. This leads to an accumulation of K in the cell which needs to be secreted through a K channel on the apical side of the cell back into the tubule (very little is secreted however so net effect is reabsorption).
Describe the transporter mechanism and in the DL of LoH.
we don’t know much about this. I just wanted to add this to be complete.
Describe the transporter mechanism and characteristics in the CCT.
This will most likely be on the test
Na is brought into the cell via ENac (epithelial sodium channel) on the apical side. Then Na/K/ATPase kicks Na out and brings K in on the basolateral side. K increases in the cell and then leaves via a K channel on the apical side to enter the tubule. This is a secretory epithelium.
This is the major epithelium that regulates total body K on a day to day basis. Also, this is the epithelium that has the mineralocorticoid receptor on it. More to come on this later.
what is the role of the mineralocorticoid receptor?
receptor on the CCT epithelium that when activated by aldosterone regulates the location and abundance of the three main transporters that this epithelium contains:
- ENac
- Na/K/ATPase
- K channel
Describe the transporter mechanism and characteristics in the epithelium between the late CCT and urine (also called the medullary and papillary collecting tubule).
There is a KCl co-transporter and a K-proton ATPase. The proton transporter brings K into the cell and sends H+ into the tubule. He did not talk about the other transporter.
This is reabsorptive epithelium
We don’t need to know anything else about these.
Which of the above types of epithelium would you expect to be intercalated cells? principal cells?
intercalated- the medullary and papillary collecting tubule (secretes H+).
principal- CCT
What are the major regulators of K secretion in the CCT? What sort of states could affect those regulators?
Na and aldosterone (without Na, there is no K excretion). Also, WINK proteins but we’l talk about these later.
Is someone is volume depleted then they will absorb all the Na in the earlier parts of the tubule and none will make it to the CCT. Then you will be predisposed to hyperKalemia. There are many disease states that can do this (heart failure for instance). Also, it doesn’t matter how much Aldosterone there is, if Na is not present, the transporters do not work.
Why might a patient with heart failure start out hyperkalemic and then become hypokalemic after going to the doctor?
They are given a loop diuretic. All of a sudden lots of Na reaches the CCT and there is a bunch of aldosterone that has built up sitting there. It will secrete a bunch of K leading to hypoK.
