Lecture 8: Water Homeostasis Flashcards
how is H2O intake altered?
activation or decrease in thirst
how does the body excrete H2O and how is excretion regulated?
loss from skin, respiration, GI tract, kidney**
kidney regulates it
how much of total body water is in the ICF versus ECF?
2/3 in ICF, 1/3 in ECF
1/4 of ECF in intravascular (plasma) fluid
3/4 of ECF in interstitial (extravascular) fluid
What is the difference between osmolality and tonicity?
osmolality is the total particles per unit weight of solvent. It is measurable and calculable
tonicity is the # of particles that cannot freely cross cell membrane per unit volume (effective osmolality). it is not measurable, but is calculable
What ions play a major role in ECF?
Na - major cation
Cl-, HCO3- major anions
What ions play a major role in ICF?
K+ and Mg2+ are major cations
proteins and phospgate are the major intracellular anions
What must occur to have renal H2O excretion?
Fluid must be filtered at the glomerulus
Salt must be removed from the ultrafiltrate (thick AL of loop of Henle).
The “free” H2O must transverse through tubules that are H2O tight
What must occur to have renal H2O reabsorption?
An osmotic gradient must be generated to allow H2O to be reabsorbed.
This gradient is established by generating and maintaining a hypertonic medullary
interstitium
Vasopressin must be present to allow H2O reabsorption in the collecting duct by
increasing H2O permeability of the apical membrane (insertion of aquaporin 2).
Describe water filtration at glomerulus
H2O is freely filtered. ~150 liters of H2O are filtered daily (GFR).
Describe water reabsorption at proximal tubule
Solutes and H2O are reabsorbed isotonically by the proximal tubule. ~60% to 70% of the
ultrafiltrate is reabsorbed normally. Up to 90% reabsorption of the ultrafiltrate can occur
with severe effective circulating volume depletion.
Describe permeabilities in the descending limb of the loop of Henle
H2O permeable, and Na+ impermeable
H2O leaves the urinary space through aquaporins as the tubular fluid flows through the medulla in response to the osmotic gradient.The concentration of solutes in the tubular fluid progressively increases to a maximum value at the tip of Henle’s loop. Under conditions of severe effective circulating volume depletion, up to 90% of the H2O in the filtrate that reaches the loop of Henle can get reabsorbed in this segment. Therefore, low ECBV decreases the renal capacity for the excretion of water by activating a series of steps that enhance proximal fluid reabsorption through hemodynamic effects and a direct stimulation of transport in the proximal tubule and enhanced water reabsorption in the descending limb. It can also reduce GFR in extreme cases. The net result is a limit on the amount of isotonic fluid that is delivered
downstream to the distal diluting sites
Describe permeabilities in the ascending limb of the loop of Henle
H2O impermeable, but actively transports Na+ out of the tubule and can establish a local osmotic gradient of ~200 mOsm across the epithelial layer. This antiparallel (or countercurrent) flow of fluids through neighboring pathways generates a
hypertonic interstitium as well as hypotonic tubular fluid at the end of Henle’s loop. This process is termed countercurrent multiplication. The interstitial
osmolality varies from between 285 mOsm/kg H2O in the cortex to up to ~1200 mOsm/kg H2O in the inner medulla under conditions of maximum antidiuresis.
NaCl is transported out the tubular space, such that by the end of the loop of Henle, the osmolality of the tubular fluid is quite low (or hypotonic; ~ 50 to 100 mOsm/kg H2O).
- In the first portion of the ascending limb, the thin ascending limb, NaCl passively diffuses out of the tubular lumen. The NaCl concentration in the interstitium is lower than in the tubular lumen. Urea diffuses into the tubular lumen from the interstitium,
as the urea concentration in the interstitium is greater than in the tubular fluid.
- The latter portion of the ascending limb is the thick ascending limb. NaCl is transported
out of the tubular lumen by crossing the apical membrane via a Na/K/2Cl cotransporter. The Na+, K+-ATPase then extrudes Na+ from the cell and Cl- exits the cell via basolateral Cl- selective ion channels.
- ~ 15% - 20% of the filtered H2O is reabsorbed in the loop of Henle
Describe water reabsorption at the distal convoluted tubule
Largely H2O impermeable. Vasopressin will increase H2O permeability of the late distal
convoluted tubule. As NaCl is transported out the lumen, the osmolality of the tubular fluids may decrease further.
Describe water reabsorption at the collecting duct
The collecting duct is the final site of H2O reabsorption by the kidney.
Without vasopressin, the apical membrane is H2O impermeable.
The final urine osmolality can be as low as 50 mOsm/kg H2O. Up to 18 liters of free H2O exit the loop of Henle.
In the continued absence of vasopressin, H2O excretion by the kidney can approach levels of 18 liters/day.
In the presence of vasopressin, H2O permeability of the apical membrane is increased by the movement of water channels from a cytoplasmic pool to the cell surface. In the cortical collecting duct, the tubular fluid osmolality can rise up to ~300 mOsm/kg. The cortical collecting duct is largely impermeable to urea. As the tubular fluid flows through the medullary collecting duct, both H2O and urea can be reabsorbed in the presence of vasopressin by passive diffusion. The final urinary
osmolality can reach levels as high as 1,200 mOsm/kg H20.
Describe urea reabsorption at the collecting duct
Urea diffuses out of the medullary collecting duct and contributes to the osmolality of the
medullary interstitium and during states of active water reabsorption by the kidney, can
account for up to 40-50% of the solutes in the medullary interstitium. Vasopressin
activates urea transporters in the medullary collecting duct that facilitate the transport of
urea out of the tubular lumen and into the medullary interstitium. In the absence of
vasopressin (e.g., chronic ingestion of large volumes of water, diabetes insipidus)
medullary urea concentration drops, decreasing the ability of the affected individual to
form a concentrated urine.
