L15- Potassium homeostasis

where is most of K in our body

In muscle 2600 mmol

Functions of K

Trancellular (difference in K inside and out)

• maintian resting portential

• cardiac pacemaker

  • neuromuscular excitability

Intracellular (high K levels inside than outside)

• pH regulation

• cell vol maintance

• cell enzyme reactions

what is it called when have too high or too low K levles

too high → hyperkaleimia

too low → hypokaleimia

K homeostasis

• absorbe by GI tract same amount of K in ECF ~70mmol

• short term use this absorbed to buffer amount of K in ECF by liver, muscle, bone, RBC → traslocation

• long term excess K is excreated by kidenys - excreate same anoynt of K we injest

• helps keel K in ECF within narrow range

why is K regulation important

• when have incraesed plasma K leads to absormal rhythm in gthe heart - heart doesnt beat correctly

• lcan lead to death so need to have tightly regulated K levles

what can chnage K homeostasis

• eating highly K foods like bananas eating a lot is dangerous

• K loss → urine, GI tract by diareahha, burn paitenst low K conc in ECF

• redictribution of K between fluid compartments → cell lysis all K in cells lost, exercise, plasma osmolarity

Intestinal K absorption

• 85% of ingested K absorbed

• have paracellular absoption of jejonum and ileum

• can also have tracellular absorption by distal colon in cases when injest low K can scavange nad loow for it here

• in usuall cases kidney able to adapt to high K intake GI is not regulated under normal physiological conditions

K absorption in jejunum and ileum

K absorption in distal colon

what happens to the absorbed dietry K levles after a meal

can cause ECF K levles to double very quickly so

1- get traslocation mainly into skeltal msucle within minutes (then release K after 2-14h after meal)

2- kidney excreation - 90%

3- Gi excreation 10%

what hormones are important in traslocation

Insulin → glucose in a meal triggers B cells to secraete insulin, inslin acts on msucle cells to uptake K

Adrenaline → repeated AP cause K to be release form cell, adrenlaine helps uptake fo K by cells to maintain ECF conc

Aldrestrone → dont knwo the mechnism but its important

Tralocationa nd insluin

• After a meal get increase in Insulin

• Na/K ATPase higest abundance in skeletal msucle

• Insulin binding to recptor on skesltal msucle calsues incraese abundance of NA/K ATPase by increasing membarne tarfficning

• also causes phosphrylation of FXYD1 (normally inhibts NAk atpase) leading to increase function of NA/KATPASE

• more K moves itno cell minutes after eacting

role of adrenaline in traslocation

• when muscle contracting alot release K inot ECF

• adrenlaine also reciced during exercise

• binds to its recptor cuasing increase in cAMP and so more Na/KATPase to move to the surface so more K into the cell

• so get tarslocation of K within minutes

where is the K absorbed in kidey

proximal tubule (most) 70%

Think asending limb 25%

distal tubule 10% → secreations - when have too high K in blood

REabsorption in proximal tubule

reabsorption in thick assending limb

K secreation in distal tubule

what does aldestrone do

• binds to minero cortico reseptor

• activates SGK1

• increases membarne proetins levels

K secreation in clolon

• NKCC1 brings K from blood into cell

• BK channel allows K into lumen more K excreated

• aldestrone enhances it but cannot incraese K secreation by alot