Lecture 6: Water transport in the kidney II Flashcards
What is the countercurrent system in the kidney? what is its function
he process of using energy to generate an osmotic gradient that enables you to reabsorb water from the tubular fluid and produce concentrated urine.
where does the countercurrent mechanism occur in the kidney
loop of Henle
describe the anatomy of the loop of Henle
- descending - permeable to water, impermeable to ions
- ascending - impermeable to water, highly permeable to sodium
- establishes osmotic gradient; allows varying urine concentration
- basolateral surface faces interstitium
- apical surface faces lumen
- surrounded by peritubular cappillaries aka. vasa recta
- reabsorption/secretion to and from blood via interstitium
why is the ascending loop of henle impermeable to water
due to it having no aquaporin channels
describe the anatomy and physiological features of the descending loop of Henle
- filtrate that enters has osmolarity of ~300 mOsm/L
- squamous epithelial cells have aquaporins on either surface
- water moves via osmosis into the interstitium
- osmolarity can reach 1200 mOsm/L at bottom of loop
what does countercurrent multiplication refer to
process of creating a concentration gradient along the loop of Henle, it uses ATP
describe the anatomy and physiological features of the thin ascending loop of Henle
- no aquaporins but sodium and chloride channels instead
- move from lumen to interstitium along CG
- osmolarity can decrease to ~600 mOsm/L at top of thin loop
describe the anatomy and physiological features of the thick ascending loop of Henle
- cuboidal epithelium
- Na/K/Cl cotransporter
- Na+ K+ and 2Cl- moved from lumen into cells using Na+ concentration gradient
- Na/K ATPase working to generate energy
- K+ and Cl- move into interstitium from cell down their concentration gradients
- osmolarity can decrease to ~325 mOsm/L at top
why “countercurrent” “multiplication”
countercurrent - because descending and ascending limb go in opposite directions
multiplication - when we reabsorb ions in the ascending limb and make the medulla salty, by not reabsorbing water, that drives water to be reabsorbed passively in the descending limb
use energy to reabsorb ions in ascending limb - active transport
water reabsorption is passive
what are the basic requirement for forming concentrated urine?
- a high level of antidiuretic hormone
- a high osmolarity of the renal medullary interstitial fluid which provides the osmotic gradient necessary for water reabsorption to occur
how does the renal medullary interstitial fluid remain hyperosmotic
due to the countercurrent mechanism
using sodium transporters, the loop of henle can establish a difference of ____ mOsm/L between the loop and the interstitium
200
what is the term reffered to that allows water to move from the descending limb into the interstium due to an increase in sodium concentration
osmotic pressure to drive water out of the descending limb
what is the purpose of water movement out of the descending limb? what is the consequence of this?
to make the concentration of sodium ions equal in the interstitum and descending loop of henle
causes filtrate to become more concentrated/sodium concentration increases in the descending loop of Henle because youre removing water
filtrate keeps moving along, same process occurs making it more and more concentrated until we reach maximmum concentration in the medulla - 1200 mOsm/L
NaCl transport generates only a —- gradient across any portion of the ascending limb, but countercurrent exchange can multiply this single effect to produce a —- gradient between cortex and papilla
~200-mOsm
900-mOsm
What is a single cycle in the countercurrent mechanism made up of
“single effect” - generates a 200 mOsm gradient by NaCl transport from lumen of ascending limb to the interstitium and water equilibrating this change from descending loop
“axial shift” - movment of tubule fluid along loop of Henle with an instantenous equlibration between the lumen of descending limb and the interstitum
what is antidiuretic hormone
- peptide hormone prevents excessive urine production by reabsorbing water from the kidneys
- it allows the body to control the amount of fluid retention
What triggers ADH (aka vasopressin) production
- osmoreceptors in anterior hypothalamus, baroreceptors in CV system; stimulated by angiotensin II
- causes smooth muscle cells in arteries to constrict
How does ADH reach the kidneys from the hypothalamus
- produced in anterior hypothalamus
- stored in posterior pituitary
- when needed, released into blood, travels to kidneys
- binds to AVPR2 receptors on basolateral membrane of principal cells along collecting ducts of nephrons
- AVPR2 signals adenyl cyclase to convert ATP to cAMP –> cell produces aquaporins, opens existing aquaporins in apical membrane, osmosis pulls water from lumen of ducts into interstitium, reabsorbed into circuclation
what is the main function of ADH
- increase water permabiltiy of distal tubule, collecting duct and collecting duct epithelia
- conserve water
- triggered by decrease in water excretion
explain the process of osmoreceptors firing
- Osmoreceptros, cell body located where blood brain barrier is leaky – sample plasma going past
- Specialised – shape and structure is resposive to changes in osmolarity, changes in cell shape triggers change in activity
- Increased osmolarity – more osmoles in plasma, water leaves osmoreceptor, change in shape, causes it to fire, depolarise, adh released, to plasma to kidney
Why is it crucial to have adequate amounts of ADH in the body
low - can get central and nephrogenic diabetes insipidus
high - hyponatremia
central diabetes insipidus
- decreased release of ADH from neurohypophysis
- can be due to impaired synthesis in the hypothalamus, impaired transport to the neurohypophysis, or impaired storage and secretion from the neurohypophysis
nephrogenic diabetes insipidus
- plasma ADH levels can be normal but response of the collecting duct to the hormone is depressed
diabetes insipidus in general refers to what?
a condition where synthesis, secretion or action of ADH is impaired resulting in polyuria - production of large amounts of dilute urine
how is central diabetes insipidus treated
administration of exogenous ADH
hypernatremia
too much sodium in the blood
how is hypernatremia related to ADH
plasma osmolarity high, osmoreceptors sense this, release of ADH to kidneys
hyponatremia
when the concentration of sodium in your blood is abnormally low
give a possible reason for hyponatremia
excessive fluid intake - polydipsia
- degree of hyponatremia depends on the level of fluid intake relative to renal water excretion
what is maximal diuresis in a human
18-20 L/d
what happens if fluid intake exceeds maximal excretory capacity?
a reduction in plasma Na+ concentration must occur
How would you distinguish between diabetes milletus and central/nephrogenic insipidus?
urine glucose levels