Urine Concentration and Dilution

Urine Concentration and Dilution

characteristics of hyperaldosteronism

• High MAP - increased Na+ reabsorb increases blood volume

• hypoalemia - low potassium

• alkalotic - blood has low acid

water balance

• input - diet (main) and metabolism

• output - urine (main), lungs, skin and feces

negative water balance

output greater than input - most obvious thru increased ECF osmolarity bc more solutes than water

how are changes in water balance detected

thru osmolarlity changes via osmoreceptor cells in anterior hypothalamus - stimulated by changes in cell size

• low water = cells shrink

what responses will a negative water balance cause

• concentrated urine to increase water retention

• thrist

what is needed to produce concentrated urine

vasopressin/anti-diuretic hormone - makes collecting ducts more permeable = more water reabsorbed

relationship between vasopressin and osmolarity

vasopressin increases when osmolarity increases

vasopressin and ECF volume

under normal conditions vasopressin doesn’t care about ECF volume bc that relates more to Na+

• if ECF gets too low = vasopressin increases

water and the nephron

• proximal tubule = bulk absorption

• ascending limb = dilution of filtrate

• collecting ducts = fine-tuning according to needs

minimum solute and water needed to be excreted per day

• 600 mOsm of solute

• 500ml of water

tubular fluid leaving the loop of Henle is normally

1. dilute

2. isomotic

3. concentrated

dilute bc ascedning limb is impermeable to water but permeable to NaCl

fluid thru loop of henle

1. exits proximal as isomotic (300 mOsm/L)

2. descending limb goes deeper into renal medulla

3. descending permeable to water but not solutes

4. 1200 mOsm/L at bottom of loop

5. thick ascending limb impermeable to water but permeable to solute

6. 100 mOsm/L as entering distal tubule

7. hormones control distal permeability to water and solutes

renal medulla and osmolarity

deeper into renal medulla = higher osmolarity = ECF outside of nephron becomes more concentrated

what part of nephron does urine osmolarity depend on

reabsorption in collecting duct

The medullary concentration gradient is mostly the result of

urea (main) and sodium

thick ascending limb of loop of henle

permeable to solute and impermeable to water

how are solutes reabsorbed in thick ascending limb

1. passive transporter on luminal membrane NKCC2

2. NKCC2 moves 1 Na+, 1 K+ and 2 Cl- into loop cells

3. Na+/K+ ATPase pumps Na+ into interstitial

4. Cl- channels into interstitial

loop diuretics

drugs that inhibit NKCC2 cotransporter = blocks solutes from leaving filtrate = decreases water reabsorb = increase urine volume

• also decrease NaCl in medulla = decrease medulla osmotic gradient = decrease ability to concentrate urine

what is needed to produce concentrated urine

• NKCC2 cotransporter

• aquaporin 2

• cAMP

how does vasopressin increase urine concentration

1. vasopressin binds to membrane receptor on outer membrane of collecting duct

2. activates cAMP second messenger

3. storage vesicles insert aquaporin-2 into luminal membrane = pores

4. water moves osmotically from lumen into blood

what is the max urine osmolarity

1200 mOsm

importance of medullary concentration gradient

allows kidney to make concentrated urine

• greater medullary concentration = greater water reabsorb = higher urine osmolarity