K+ Balance Flashcards
Plasma K concentration is a function of what?
Internal and external K balance
Chronic changes in K concentration due to?
External balance issues
Acute changes in K concentration due to?
Could be both internal or external
How does the body handle acute K load?
Increase in cellular k uptake and enhanced renal k excretion
-About 75% is taken up into the cells followed by a relatively rapid excretion of K
Can urinary excretion exceed the filtered load of k?
Yes, due to tubular secretion
Primary defense against progressive K depletion and hypokalemia?
Renal K reabs. This is slow and can take days to develop so a substantial K deficit can occur in the meantime (unlike Na)
What is the major regulator of internal K balance?
Na-K ATPase
What factors affect internal K balance?
- Plasma K concentration
- Hormones (insulin, catecholamines, aldosterone)
What factors stimulate Na-K-APTase activity?
- High plasma [K]
- Acute increase in plasma K stimulates insulin, aldosterone and catecholamine release which all favor K cellular uptake (also have passive diffusion into the cells)
Catecholamines effects on K
-Stimulate insulin
-Work on beta 2 to increase Na-K ATPase activity and lower plasma K concentration
-
Aldosterone effects on K
Stimulates Na-K ATPase activity and distal nephron K secretion and urinary excretion of K
Effect of exercise on plasma K
Increase
Effect of cell lysis on plasma k
Increase
Effect of alkalemia on plasma k
K+ enters the cell –exchanges with H+
Effect of acidemia on plasma K
K+ leaves the cell–exchanges with H+
Effect of intracellular acidosis on plasma K
- Decreased intracellular pH inhibits K+ uptake, lowering intracellular K
- This displaces K+ for exit from the cell (ie increase in K+ out of the cell)
Acidosis inhibits Na-K pump and N2CCK
Effect of plasma tonicity on plasma K
Hypertonic plasma: K+ follows water via drag and K passively leaks out due to cell shrinkage
-glucose increases hypertonicity in diabetic patients causing K+ plasma to increase. In non diabetics, insulin causes uptake of K+ into cells (follows water and stim Na-K)
How would you describe the filtration of k
it is freely filtered
-fractional abs of 80% in the PT and 10% in the TAL is constant regardless of K balance so reabs at these sites is not a major determinant of final renal k excretion
How much of filtered K is delivered to distal nephron?
About 10%
How is K reabs in the PT?
Through paracellular pathways in response to Na reabs-induced fluid movement
Late PT: positive transepithelial potential difference also drives this
Luminal K channels are only minimally conductive in the PT
How is K reabs in the Thin descending limb?
-Deep juxtamedullary nephrons in the medulla passively secrete K into the lumen from the interstitium
How is K reabs in the Thin ascending limb?
K passively moves from cell to interstitium
How is K reabs in the TAL?
- Passively due to luminal potential difference
- Actively with NKCC2 with ROMK recycling or BLM diffusion
Alpha intercalated cells of the cortical collecting duct and outer medullary collecting duct?
Reabs K
- Make up <30% of cells here
- H-K ATPase actively reabs K across apical membrane and basolateral K channel for K efflux from the cell
Principal cells of the cortical collecting duct and outer medullary collecting duct?
Secrete K
- make up >70% of cells here
- Apical K channels and Cl-K co transporter
- Negative potential difference in this region favors Na reabs and tehrefore K transport
Factors affecting distal nephron K secretion
- K intake and plasma K concentration
- Aldosterone
- Distal tubule Na delivery and flow
- Anions in tubular fluid
Aldosterone effect on K
Stimulates principal cell transport processes
-note glucocorticoids dont directly affect renal K secretion
