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Tubular secretion and renal handling of potassium. Stephen P. DiBartola, DVM Department of Veterinary Clinical Sciences College of Veterinary Medicine Ohio State University Columbus OH 43210. Terminology Transepithelial versus transmembrane potential difference

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tubular secretion and renal handling of potassium
Tubular secretion and renal handling of potassium

Stephen P. DiBartola, DVM

Department of Veterinary Clinical Sciences

College of Veterinary Medicine

Ohio State University

Columbus OH 43210

slide2

Terminology

Transepithelial versus transmembrane potential difference

Luminal versus basolateral membranes

Transcellular versus paracellular transport

slide3

Just think

of it as a

six-pack

Luminal surface

Epithelial tight junctions

Basolateral surface

substances secreted by the renal tubules
Substances secreted by the renal tubules
  • Weak acids (organic anions) or weak bases (organic cations)
  • Foreign substances (e.g. drugs, PAH, PSP)
  • Substances that are not metabolized and excreted unchanged in the urine (e.g., PAH, PSP)
  • Substances that are slowly metabolized (e.g. thiamine)
evidence for tubular secretion psp
Evidence for tubular secretion: PSP
  • 70% of a dose of PSP is excreted after a single circulation through the kidneys
  • 75% of PSP is bound to plasma proteins (25% is free and available for filtration)
  • If FF = 20%, only 5% of dose can be filtered in one circulation through the kidneys (20% of 25%)
  • 65% of dose must have gotten into the urine by secretion (70% - 5%)
normal plasma constituents that undergo secretion at specific sites in the renal tubule
Normal plasma constituents that undergo secretion at specific sites in the renal tubule
  • Hydrogen ions
  • Ammonium
  • Potassium
  • Urate
renal handling of potassium
Renal handling of potassium
  • Kidneys are the primary regulator of potassium balance
  • Potassium is the only plasma electrolyte that is both reabsorbed and secreted by the tubules
renal handling of potassium1
Renal handling of potassium
  • Independent of state of balance
    • 60% reabsorbed passively in proximal tubule
    • 20% reabsorbed in thick ascending limb of Henle’s loop via Na+-K+-2Cl- carrier
  • Dependent on state of balance
    • Secretion by principal cells in cortical collecting duct and outer medullary collecting duct
    • Reabsorption by H+-K+ ATPase in Type A () intercalated cells in inner medullary collecting duct
renal potassium handling proximal tubule
Renal potassium handling: Proximal tubule
  • Early proximal tubule
    • TEPD lumen negative
    • K+ reabsorbed with water by solvent drag
  • Late proximal tubule
    • TEPD lumen positive
  • Paracellular route important
renal potassium handling thick ascending limb of henle s loop
Renal potassium handling: thick ascending limb of Henle’s loop
  • TEPD lumen positive
  • Paracellular route important
  • Basolateral exit via K+ channels and K+-Cl- cotransporter
renal potassium handling late distal tubule and collecting duct
Renal potassium handling: Late distal tubule and collecting duct
  • Principal cells responsible for K+ secretion
  • TEPD lumen negative
renal potassium handling late distal tubule and collecting duct1
Renal potassium handling: Late distal tubule and collecting duct
  • Type A () intercalated cells reabsorb K+ and secrete H+
  • K+ enters at luminal membrane by H+-K+ ATPase
  • K+ exits at basolateral membrane by K+ channel
major factors affecting k movement across cortical collecting duct epithelium

Think of it like a river

Major factors affecting K+ movement across cortical collecting duct epithelium
  • Chemical concentration gradient for K+ across luminal membrane
  • Distal tubular flow rate
  • Transmembrane PD across luminal membrane
factors influencing renal excretion of potassium
Factors influencing renal excretion of potassium
  • Sodium intake
  • Potassium intake
  • Mineralocorticoids (i.e. aldosterone)
  • Hydrogen ion balance
  • Diuretics
increased sodium intake
Increased sodium intake
  • More Na+ reaches distal tubules and enters cells across luminal membranes stimulating Na+-K+ ATPase in basolateral membranes and increasing intracellular K+ concentration
  • Increased distal delivery of Na+ increases tubular flow rate and moves secreted potassium downstream
increased potassium intake
Increased potassium intake
  • Increased numbers and activity of Na+-K+ ATPase and amplification of basolateral membranes secondary to aldosterone secretion
  • Increased Na+-K+ ATPase activity increases intracellular K+ concentration favoring secretion
aldosterone stimuli for release
AldosteroneStimuli for release
  • Volume depletion RAS activation Angiotensin II stimulates zona glomerulosa of adrenal gland to release aldosterone
  • Hyperkalemia also stimulates zona glomerulosa
  • Other (minor) stimuli
    • ACTH
    • Hyponatremia
    • Decreased extracellular pH (acidosis)
aldosterone effects
AldosteroneEffects
  • Main effect is to increase the number of open Na+ channels in luminal membranes of principal cells
  • Also stimulates H+ ATPase in luminal membranes of Type A () intercalated cells
aldosterone inhibition of release
AldosteroneInhibition of release
  • Dopamine (released in response to increased ECF volume)
  • Atrial natriuretic peptide (released in response to increased ECF volume)
nephron segments affected by aldosterone
Nephron segments affected by aldosterone
  • Connecting segment (late distal tubule)
  • Cortical collecting duct
  • Outer medullary collecting duct
slide21

Could you remind me again … what are the parts of the nephron?

… What a bozo …

Glomerulus…

Proximal tubule…

Thin descending LH…

Thin ascending LH…

Thick ascending LH…

Distal convoluted tubule…

Connecting segment…

Cortical collecting duct…

Outer medullary collecting duct…

Inner medullary collecting duct…

hydrogen ion balance
Hydrogen ion balance
  • Alkalosis increases urinary excretion of potassium
  • ACUTE MINERAL METABOLIC acidosis decreases urinary excretion of potassium
    • ORGANIC METABOLIC acidosis does not
    • CHRONIC METABOLIC acidosis may increase urinary excretion of potassium
effects of acid base balance on translocation of potassium
Effects of acid base balance on translocation of potassium

H+

K+

K+

H+

ACIDOSIS

ALKALOSIS

An oversimplification in acidosis

diuretics
Diuretics
  • Many diuretics increase urinary excretion of potassium (e.g. furosemide, thiazides, mannitol)
  • They do so by increasing distal delivery of sodium and distal tubular flow rate
renal handling of urate
Renal handling of urate
  • In veterinary medicine, primarily important in Dalmatian dogs
  • Urate is both reabsorbed and secreted in the renal tubule
  • Secretion resembles that of PAH
    • Co-transported into cell with Na+ at basolateral membrane
    • Exits cell at luminal membrane by facilitated diffusion down its concentration gradient