Unit 7 - Regulation of Potassium Flashcards
how is K+ related to H+?
[K+] participates in pH regulation, due to effective K+/H+ exchange across cell membrane
extracellular VS intracellular K+ concentrations
extracellular: 3.5-5.0 mM
intraceullar: 120 mM (98% of total body K+)
how is K+ related to the cell voltage?
major determinant of cell voltage of [K+] gradient
- if extracellular K+ increases, the gradient decreases, so voltage depolarizes (less negative)
- if intracellular K+ increases, gradient increases, so hyperpolarizes (more negative; this is what it is usually)
how is K+ important in excitable and unexcitable cells?
K+ gradient across cell membrane is major determinant of potential in both types of cells
-in excitable (cardiac, neural, muscle), the currents are central to property of “excitability”
what defines hyperkalemia?
plasma [K+] above 5.0 nM
- decreases outwardly directed K+ gradient
- resting membrane potential is depolarized
- -muscle hyperexcitability
- -cardiac conduction disturbances (ventricular arrythmia and fibrilation, tachycardia)
- metabolic acidosis (since K+ enters cells, H+ exits cells)
what defines hypokalemia?
plasma [K+] below 3.5 mM
- increases outwardly directed K+ gradient
- resting membrane potential is hyperpolarized
- -muscle hypoexcitability
- -cardiac pacemaker disturbance (arrythmia, bradycardia)
- metabolic alkalosis (since K+ exits cells, H+ enters cells)
K+ balance and distribution throughout body (external VS internal VS kidney) daily
external: GI uptake (100 mmol)
- 10 mmol in feces
- 90 mmol to ECF
internal: ECF constant at 65 mmol (4.5 mM); exchange with organs
- muscle: 2600 mmol
- liver: 250 mmol
- bone: 300 mmol
- RBC: 250 mmol
kidney: 90 mmol excretion = 810 mmol filtration + 50 mmol secretion - 770 mmol reabsorbtion
what is the first line of defense against hyperkalemia? what is the one cell that doesn’t participate in this?
increased uptake of [K+] into cells
- acute increase in plasma [K+] triggers release of insulin (pancreatic beta cells), epinephrine (adrenal medulla chromaffin cells), and aldosterone (adrenal cortex glomerulosa cells)
- these all act to activate K+/N+ ATPase, such that K+ can enter cells and Na+ can exit cells
since RBC don’t have a nucleus or the ability to respond to the above hormones, they don’t participate in this response
how is hyperkalemia related to diabetes?
since insulin is released in response to acute increases in [K+], poorly-controlled BM may compromise tolerance of diabetes patients to K+ load, and predispose them to hyperkalemia
why does acidemia cause hyperkalemia?
acidemia inhibits the Na/K ATPase and Na/K/2Cl cotransporters, which lowers intraceullar [K+] and causes K+ loss from cells
-also, H+ enters cells and K+ exits cells via K+/H+ antiport
how does alkalemia stimulate hypokalemia?
alkalemia stimulates Na/K ATPase and Na/K/2Cl cotransporters, so more uptake of K+ into cells, causing hypokalemia
how does the body handle K+ after an acute K+ load?
plasma K+ will slowly decrease back to baseline due to:
- initially high net cumulative translocation of K+ into cells (slowly tapers off)
- slowly increasing cumulative renal excretion of K+ above baseline
how does K+ reabsorption in proximal tubule change at low, normal, or high plasma K+ levels? in the distal tubule?
PT: IT DOESN’T; reaborption is constitutive (not regulated) in proximal tubule
-it’s always most of the filtered K+ (~80%)
DT: either reabsorbs or secretes K+, depending on K+ balance and plasma K+ levels
K+ handling when dietary K+ intake is low and K+ balance is negative
- 80% reabsorbed in proximal tubule constitutively
- 10% reabsorbed in TAL constitively
- since low K+: 2% reabsorbed in collecting tubule + 6% reabsorbed in medullary collecting duct
- remainder: 2% of filtered load is remaining for excretion
what is an instance where hypokalemia can result, despite compensating increase in K+ reabsorption by distal nephron?
chronic dietary K+ deficiency
