Regulation of K balance Flashcards
(21 cards)
Counterion of K
phosphate or sulfate, not chloride. Phosphate and sulfate are poorly resorbed in distal tubule and collecting duct. Some organic ions can be turned into HCO3-, and HCO3- in collecting duct facilitates potassium excretion.
[K plasma]
3.5-5.0 meq/L
Functions of intracellular K
Maintenance of cell volume (direct relationship) Necessary for RNA/protein synthesis (deficiency = stunted growth) Regulates acid/base balance (loss = acidosis, gain = alkalosis) Maintains membrane potential Cofactor for some enzymes Vascular function (low K = vasoconstriction, and opposite)
Insulin
Brings glucose into cells,
Increases Na uptake bc it needs phosphate from Na/phosphate symporter
Pulls K out of blood
Can cause hyperkalemia right after starvation
Epinephrine via B2-receptors
B-receptors increase Na-K ATPase activity, pulling more K into the cell and possible producing hypokalemia, limits K going out
Norepinephrine via alpha-receptor
Causes K to shift out of cells, minimizes hypokalemia after exercise, limits K coming in
Hypertonicity
Causes K to exit cell
Exercise
Shifts K out of cells, where it functions as vasodilator
Someone treated with B-adrenergic antagonists can experience hyperkalemia after exercise
External K intake
Low K diet reduces transcription of Na/K ATPase (less K going into cells)
High K diet increases transcription of Na/K ATPase
All intake of K is excreted by kidney
Regulation of K absorption
85% is resorbed in proximal tubule. This is also primary site of regulation.
Effects of Acid/Base balance on K
Mineral acids cause K to shift out of cells
Organic acids have minimal effect
Effect of intracellular K on action potential
hypokalemia makes threshold potential more negative
hyperkalemia makes threshold potential less negative
Effect of Ca+2 on excitability
Hypercalcemia raises threshold potential
K secretion in nephron
K is secreted predominantly in proximal collecting duct but also in distal tubule
Ion transport In TALH
K is taken up by Na/Cl/K transport on lumen side and ejected into lumen again via K channel. K also comes into the cell by Na/K ATPase on basolateral membrane
Ion transport in collecting duct
Principal cells take in Na and secrete K via different channels, but Na/K ATPase on basolateral side connects the two events. Increasing Na resorption/K secretion also increase paracellular diffusion of Cl
Effect of flow rate on K secretion in collecting duct
High flow means more K secretion
Higher sodium delivery = more K secretion
Effect of ADH on K secretion
With no ADH, CD is impermeable to water and has high flow, maintaining high K secretion
ADH slows passage of water but also stimulates K secretion so there is no net change
Acid-Base effects on K secretion
Acidosis in CD causes principal cells to decrease K secretion.
Alkalosis in causes principal cells to increase K secretion
alpha-intercalated cell
Cell in CD that secretes H+ in exchange for K resorption
If Principal cell secretes more K, alpha-intercalated cell will pick up the extra K and secrete H
Aldosterone
Hyperkalemia directly cause Aldosterone secretion, which increases K secretion
If aldosterone release is prompted by Na deficiency, Na resorption in nephron segments proximal to CD, leaving K secretion unchanged