Potassium Balance
Potassium Reabsorption and Secretion
"Excitable" tissues:
Rely on the potassium concentration gradient across cell membranes to establish resting membrane potentials.
Excitable tissues include: nerve, skeletal muscle, and cardiac muscle.
Two key forms of potassium balance:
Internal: Describes potassium distribution between the intra- and extracellular fluid compartments.
External: Describes the relationship between dietary intake of potassium and its renal excretion.
Internal Balance
Homeostasis
ICF contains 98% of body's total K+; ECF contains 2%
Sodium-potassium ATPase (aka, pump) maintains this homeostatic internal potassium balance.
Shifts in internal potassium balance can cause cardiac arrhythmia and muscle weakness.
Hypokalemia
Reduced extracellular potassium concentration.
Potassium moves into the cell, so the intracellular potassium concentration increases and extracellular concentration increases.
External imbalance can cause hypokalemia from an increased potassium excretion-to-intake ratio.
Causes of increased intracellular concentration, include hormones, medications, and disease states.
– Metabolic alkalosis
– Diarrhea-induced loss of potassium.
– Medications
– Hormones, such as:
Aldosterone, which acts on the kidney's reabsorption of potassium (an external balance mechanism).
Beta-2 adrenergic stimulators and insulin, which drive potassium into the cell (an internal balance mechanism).
Clinical correlation:
A rapid correction of hyperkalemia (elevated extracellular potassium) can be achieved with:
– An albuterol inhaler (a beta-2 adrenergic stimulator)
– insulin, which drives potassium from the plasma into the cell (an internal mechanism)
– Kayexylate, which produces a diarrhea-wasting of potassium (an external mechanism)
Hyperkalemia
Increased extracellular potassium concentration
Potassium moves out of the cell – intracellular potassium concentration decreases and extracellular concentration increases.
External imbalance can cause hyperkalemia from a reduced potassium excretion-to-intake ratio.
Specific causes include:
– Metabolic acidosis.
– Cell lysis (when the cell bursts, its contents are released) (an internal balance mechanism)
– Increased ECF osmolarity (water will exit the cell, "dragging" potassium with it) (another internal balance mechanism)
– Medications, such as:
ACE Inhibitors, which acts on the kidney's reabsorption of potassium in the opposite manner as aldosterone (an external balance mechanism).
Beta-blockers prevent potassium entry into the cell (the opposite of beta-adrenergic stimulators).
Clinical correlation
Chronic kidney failure patients (who can't excrete potassium) can develop hyperkalemia if they become constipated: they rely on the GI tract for external balance of potassium.
External Balance
Alpha-intercalated cells: Low Potassium Levels
When dietary K+ intake is low, alpha-intercalated cells conserve potassium In the distal nephron.
Potassium is reabsorbed down the electrochemical gradient created by hydrogen-potassium ATPase (aka, pumps).
The hydrogen-potassium ATPase on the luminal membrane moves hydrogen to the tubule lumen while sending potassium into the tubule cell.
Potassium then diffuses through the basolateral membrane into the interstitium and capillaries.
Principal cells: High Potassium Levels
When dietary intake is high, principal cells return excess potassium to the tubular lumen.
Principal cells secrete potassium down the electrochemical gradient created by sodium-potassium ATPase.
Sodium-potassium ATPase moves potassium from the blood into the cell, while projecting sodium from it.
Potassium then diffuses out of the cell, into the lumen to be excreted in the urine.