Renal Concentrating Mechanism & Osmoregulation

What is the role of renal concentration gradient & osmoregulation?

Renal concentration gradient: permits H2O reabsorption, regulates H2O excretion & thus body fluid osmolality. Osmoregulation: to maintain constant osmotic pressure through control of H2O excretion (ADH) & thirst

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What is osmolality?

Number of solute particles in 1kg of water

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What is osmolarity?

Number of solute particles in 1L of water

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How does countercurrent multiplication generate a medullary concentration gradient?

Henle's loop: parallel limbs, fluid flows in opposite direction; different permeabilities to NaCl & H2O creates vertical osmotic gradient. Primary force: active transport NaCl in asc thick limb (hyperosmotic) -> H2O reabsorbed from descending limb

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What happens to fluid in the descending limb of the loop of Henle?

Fluid equilibrates with interstitial fluid -> as tubular fluid moves down it gets progressively more concentrated (as does medullary interstitial fluid to the same degree)

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Explain the equilibration process in the medullary countercurrent multiplier system

Tubular fluid at proximal tubule=plasma=renal interstitium. AL: active reabsorption of NaCl into interstitium, limiting gradient established, osmolality difference. DL permeable to H2O which diffuses out into interstitium, osmolalities equal

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How does urea trapping/recycling generate a medullary concentration gradient?

IMCD: ADH increases permeability to urea, concentrates urea by reabsorbing H2O. Urea diffuses passively (via UT1) out into interstitium, trapped in thick loop. Reabsorbed urea is half of medullary interstitial osmolality that drives H2O reabsorption

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Summarise what happens during regulation of urine concentration in proximal tubule & loop of Henle?

PT: solute/H2O permeable, osmotic/oncotic pressure, H2O reabsorption, isosmotic. DL: v permeable to H2O (reabsorbed), hyperosmotic. Thin AL: H2O imperm, NaCl out, dilutes urine, urine in. Thick AL: reabsorb NaCl, dilute fluid, hyposmotic

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Summarise what happens during regulation of urine concentration in distal tubule & collecting duct?

Early DT: active dilution, H2O impermeable, actively reabsorbs salts, osmolality falls. Late DT/CD: fluid hyposmotic, -ADH->diuresis, +ADH->increase H2O perm, AQP2 insertion, increases [urine]. IMCD: ADH increases urea permeability -> urea recycling

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What are vasa recta? What is their function?

Supply nutrients/O2 to juxtamedullary nephrons & remove excess H2O/solutes. Countercurrent exchangers & low blood flow rate prevent dissipation of gradient by washout. Descending VR: H2O diffuses out & solutes in (reversed in ascending)

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What happens when ECF osmolality decreases & increases?

If ECF osmolality decreases (excess water intake) -> water moves into cells -> swell. If ECF osmolality increases (water loss, salt intake) -> water moves out of cells -> shrink

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What mechanisms are used to regulate water intake & excretion?

Thirst: stimulates by increase osmolality (osmoreceptors) & decrease blood volume/pressure -> water intake. ADH: stimulate by increase osmolality & decrease blood volume/pressure -> conserve H2O (or enhance H2O excretion)

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What is the role of ADH in regulation of blood fluid osmolality?

High H2O intake: absence of ADH -> diuresis, large vol dilute (hyposmotic) urine produced. Low H2O intake/H2O lost/salt added: ADH release (antidiuresis) -> small vol concentrated (hyperosmotic) urine

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Renal Concentrating Mechanism & Osmoregulation

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