Water Balance Flashcards
Anatomical Parts of the Loop of Henle
Decending Limb (thick and thin)
Ascending Limb (thick and thin)
the thick is at the top
- it loops at various depths throughout the medulla (think juxtamedullary v cortical nephrons)
- as the medulla gets deeper to the center of the kdieny – the osmolaity of the medulla increases THUS the filterate as it loops down is exposed to higher osmolaities
How is the Osmotic Gradient maintained in the Loop of Henle?
- 3 main players (in acending loop)
- what is happening at the decending loop?
- the reabsorbtion of Na+ and Cl- during the acending loop (from the fitlerate into the interstitum of the medulla) = increases osmolality (hyperosml) in the deepest parts
this is conducted through the Na+/K+/2Cl- channels
- the acending loop of henle is imperimable to water – it cannot leave the filterate (unable to dilute the hyperosmolar interstitum)
- Urea is trapped within the interstitum (wont be reabsored at this point, adding to the hyperosmolaitiy of the interstium)
in the thick acending loop (at top) is when urea can be reabsorbed back into the filterate
Decending LoH
- allows water to leave the filterate and move into the medulla (to trey to COUNTERACT the influx of solutes in the interstitum)
- this allows for the tip of the loop of henle to be hyperosmolar
the net result
- hyperosmotic base of the loop & then the fluid entering the DCT is hypo-osmotic
In the Acending Loop of Henle, how are soultes transferred from the filterate eventually back into the capillary
- what soluates & what are their transporters
Acending Loop of Henle: responsible for taking Na+/2Cl-/K+ out of the filterate and moving it into the medullar & eventally back into the blood
Within the THICK ascending loops…
on the lumen facing side
- Na+/2Cl-/K+ transporter bring solutes from the filtrate into the tubular cells
on the capillary facing side
- Na+/K+ pumps move these ions from the cell into the capillary
- Cl- : travels from the cell to the capillary vai barttin channels (CIC-Kb)
- K+ moves out via ROMK channels
Clinical Disorder of Bartters Syndrome: improper barrtin channels cant move sodium into the blood –> thus you have a chronic loss of Na+ in the urine
- where sodium goes –> water follows thus you are hypovolemic
- this occurs due to a mutation in the transporter proteins
what is the role of the Distal Convoluted Tubule
- fine tuning of the sodium reabsorption process (very fine)
- this is monitored and adjusted but the juxtaglmoerualr apparatus via the macula densa cells
Macula Densa Cells: “sample” the glomerular blood to understand volume (pressure) and chloride, sodium contents & then adjust the reabsorbtion and filteration at the DCT
- send signal through paracrine signals to affect the afferent arteriole
decreased BP will trigger what
- indicate the RAAS system to reabsorb Na+ and excrete K+
Role of the Juxtaglomerular Apparatus
- Renin controlled by what
- what are the cells within
Renin controlled by…
- the renal sympatheic nerves (will vasoconstriction the afferent arteriole)
- intrarenal baroreceptors
- macula densa cells
Contents of the apparatus
- Macular Densa Cells: exist in a region of the DCT
- Juxta-glomerular cells (Granular): exisit in the afferent arteriole to monitor pressure
the macua densa cells and the JG cells communicate with each other
1. low pressure within the afferent arteriole is low - kidney thinks too little fluid (with low fluid – there is less Na+ & Cl- which is sensed by the macula densa)
2. this triggers renin to be secreted from the JG cells - agranular mesangial cells (Lacis): sit between the afferent and efferent arterioles & affect the avalible surface of the glomerulus
1. Mesangial cells also release renin
2. some of this renin is converted to AGII in the efferent arteriole
3. AGII: triggers a contraction of the mesanigal cells
4. this triggers efferent arteriolar contraction which increases the GFR (because youre constricting the
what is renin
who releases renin
what is the cascade
Renin: a protolytic enzyme which initiates the angiotension process
- secreted by JG cells and some mesangial cells
- it is a hormone which also acts as an enzyme (because it stimulates a direct local affect on the afferent arterioles but also leads to the production of AGII which will impact the efferent arteriole
- liver releases angiotensinogen
- angiotensinogen converted to AGI (via renin)
- AG I convereted to AGII (via ACE from lungs)
- AGII triggers the relase of aldosterone
the role of aldosterone within the kidneys after its activation from AGII
- what does it do & where in the nephron
Aldosterone: responsible for regulation of the blood pressure
- aldosterone when stimulated: will trigger a reabsorbtion of Na+ and a secretion of K+ when the pressure is too “low” as signaled way upstream by the renin via JG apparatus
Aldosterone is exerting its effect in the DCT (late 2/3) and within the (early) collecting duct
amoutn of sodium reabsorbition is small (3%) of the total amount compared to the approx. 60% of reabsorbtion which is occuring in the PCT
Aldosterone is specifically acting at what channels within the distal DCT and early collecting duct
- target is the epithelial sodium channels (ENaCs) (amiloride-inhibitable Na+ channels)
- aldosteron initiates the formation of proteins which can open these channels up
- aldosterone also increases the numer of ATPase at the location so that the ATP can be used for the Na+/K+ active transport on the baso-lateral surface
aldosterone allows ATP to get to the channel to power the exchange of Na+ in and K+ out & it helps to form the proteins that allow the ENaC channels to open
(also secreting H+ with the K+ as a co-transporter)
how is H+ secreted within the DCT?
what determines how much H+ is secreted?
what is the normal pH of urine? when is it considered acidoic
within the DCT (and the tubules) there are intercalated cells and there are principle cells
- intercalacted cells secrete H+
- principle cells secrete K+
Determiniation of Secretion of H+
- the amount of H+ that is secreted into the urine is dependent on the amount of Na+ that is reabsorbed
- the amount also depends on the metabolic state (acidotic or aklalotic) of the person
- increased H+ secretion requires buffer system
Urinary pH
- normal range: 4.5-8.0 (wide gap allows for lots of compensation for the body)
- ** a pH of urine < 4.5 is considered acidotic**
What is the collecting duct?
parts of the duct
Collecting Duct
- the last portion of the nephron
- collects the urine filterate from a variety of different DCT’s
- exists majortiy within the medulla
- where water balance comes to play
- does not play a role in solute filteration
- the collecting duct is sensitive to ADH
contains two portions
1. a cortical portion: where the tissue surrouding the duct is hypo-osmolar
2. a medullary portion: where the surroudning tissue is hyperosmotic
what is the role of ADH?
where is it released from
what does it act upon
how does it work?
ADH = anti-diueretic hormone (also vasopressin)
- secreted from the posterior pituitary gland
where does it act
- directly stimulates osmoreceptors within the brain: that signal the thirst mechanism
- directly target cells within the DCT and the collecting duct to become permiable to water
How ADH works
- ADH stimulates cells in collecting duct to allow water to be reabsorbed from the urine into the interstium and back into the blood
- as a result: the urine becomes more concentrated (less water more solutes)
Molecularly
- ADH binds with V2 receptors on the collecting duct cells
- these trigger aquaporin 2 channels to move from inside the cell (within the endosome) to the surface and reabsorb the water
a reduction in volume of blood triggers the barorecptors to stop firing –> this triggers the release of ADH to attempt to increase volume by reabsorbing water
the action of ADH is inhibited by alcohol
what is urine osmolarity
- how does ADH impact osmolarity
- how does ANF impact osmolarity
Urine Osmolarity: the concentration of soultes within a solution (the urine)
- can become as high as 1400 mosm/l which can be 5x the serum (which is 290)
- 99.7% of filtrate is reabsorbed, but the .3 which remains is what creates the concentration of urine
without ADH
- we would not be able to reabsorb the water within the urine
- thus: would create very dilute urine
- could be as low as 30 mosm/L
Role of ANF
- if there is too much fluid within the body –> triggers a release of ANF (atrial natriuretic factor)
- this triggers a reabsorbtion of Na+ from the PCT
- results in ….
- 1. GFR increased
- 2. no release of ADH
what is the Glomerular Tubule Balance
how does the Vasa Recta play a role
the amount of urine produced depends on…
1. the osmolarity of the plasma
2. the glomerular tubular balance
The counter-current system of the Vasa Recta helps ensure that the rate of reabsorbtion is slowed down to allow proper equilibruim of the filtrate and the medulla and the blood as it decends into the medulla deeped
- the decending area: NaCl and urea are reabsorbed into the plamsa & water is secreted
- the acending portion: NaCl and urea are secreted to the interstitum and water is reabsored
Overall
- the vasa recta is very slow moving with low pressure = allows for equilibration to occur
what is osmotic diuresis
- when substances (Na+ for example) fail to be reabsored
- this results in a pull of water out of the body along with them to become excreted
this happens in hyperglycemia high sugar = sugar in urine = pull water with it
what is pituitary diabetes insipidus v nephrogenic DI
a derangement of the hypothalmus – does not produce ADH
- thus, constant diuersis and no water reabsorbtion
Nephrogenic
- there is a problem with the receptors (V2) at the ADH action point within the collecting duct
- thus, ADH is released but it cant act properly
- water cant be reabsorbed
