Body Fluid Volume Maintenance Flashcards
Rule of Na balance
Input = Output
Positive Na balance
input > output
Negative Na balance
output > input
When you’re in +/- Na balance, which compartment is affected?
ECF volume will expand/contract, has nothing to do with plasma sodium concentration
**CHANGE IN NA+ IS EQUIVALENT TO ECF VOLUME
effective circulating volume is related to adequate perfusion of vascular beds (brain, heart, and other vital organs) and is dependent on these 3 factors
- cardiac output
- MAP (BP)
- vascular volume (plasma) (that gets pushed into vital organs)
ECV sensors
high pressure: carotid sinus, aortic arch, juxtaglomerular apparatus in kidney (HGA)
low pressure: pulmonary vessels, atria
Changes in ECV will be picked up by volume sensors, which then send these 4 important signals to the kidney. List the ones that respond to increases in ECV and to decreased ECV.
Increased ECV: atrial natriuretic peptide (ANP) –excretin sodium
Decrease ECV: SNS, RAAS, and ADH (from posterior pituitary)
An increase in sympathetic nervous system (increases/decreases) 5 important things
- increases cardiac output
(beta1 receptors, inotrophy, chronotropy, lusitropy) - increases vascular tone (alpha1 receptors, constricts and increases resistance on arteriole side and venous side, moves blood from venous to circular side to increase preload)
- Decreases RPF and GFR (constricts afferent arteriole, decreases glomerular pressure, decreases filtration) causes….
- decrease in NaCl excretion
- increase renin release
Function of renin, and where is it released?
angiotensinogen —renin—> angiotensin I –ACE–> Angiotensin II
renin is rate limiting step release from JG cells in kidney
3 factors causing renin release from JG cells
- SNS
- Baroreceptor type phenomenon in JG cells - increase pressure, increase stretch, alters renin release
- direct input from macula densa - sense alteration in electrolyte distribution
An increase in SNS causes an (increase/decrease) in renin release
increase in renin release
a decrease in MAP causes an (increase/decrease) of renin release
increase (decrease in MAP causes a decrease in arteriole stretch, renin is released, causing an increase in MAP, an increase in AA stretch, and a decrease of renin release)
in what situation does the macula densa cause a direct increases of renin release?
when the macula densa receives a decrease in solut delivery
what feedback loop causes a decrease in renin release?
Angiotensin II
Function of aldosterone and where in nephron and what channels
increases Na reabsoprtion in CD (principal cell)
- increases Na channel (reabsorption on apical side)
- increases K channel (increased secretion due to paracellular transport of Cl)
- increases ATPase on basal side
long term: increases the number of transporters/channels by acting on TFs
renal effects of AII
change in RPF/GFR and increases NaCl reabsoprtion in PT
extrarenal effects of AII (4)
potent vasoconstrictor, increases aldo release, increases ADH release, increases thirst
Euvolemia
normal ECV volume, input = output
major player during euvolemia
aldosterone in CD
filtered load of Na
GFR x P(Na)
The goal of maintaining constant NaCl delivery to the CD is done by these two factors
- autoregulation (MAP vs flow)
2. glomerulotubular balance
3 aspects of glomerulotubular balance that try and keep NaCl delivery to CD constant
- starling forces
- filtered load: glucose/AA
- tubuloglomerular feedback
How do starling forces contribute to glomerulotubular balance and thus constant delivery of NaCl to CD?
- if lie down, increase hydrostatic pressure of glomerular capillary, thus more gets filtered
- increased filtration causes increase in osmotic pressure in peritubular capillaries (since holding protein back)
- since also moving more fluid out, hydrostatic pressure in capillaries decreases
- favors reabsorption
how does filtered load of glucose and amino acids contribute to glomerulotubular balance?
glucose and Na are coupled with Na in symporter
-if want to reabsorb them, will also reabsorb more Na
how does tubuloglomerular feedback contribute to glomerulotubular balance?
- JGA will release renin
- signals to MD
When there is a decrease in ECV, where is the most Na reabsorbed so that the same amount is delivered to CD? Who are the major players and where are they acting on the nephron?
More absorbed in the PT/Thick descending loop
(normal is 67%, now its 75%)
TAL-will respond to amount being delivery by either increase or decreasing its capacity (normal is 25%, now it’s 15%
- glomerulus: SNS and AII increase
- PT: SNS and AII increase
- DT: Aldo increases
- CD: Aldo and ADH increase (enhances water reabsorption)
When there is an increase in ECV, where is the most Na absorbed so that the same amount is delivered to the CD? Who are the major players and where are they acting on the nephron?
Less absorbed in the PT/Thick descending loop (normal is 67%, now its 60%)
TAL goes from 25% to 30% since flooded with stuff the PT didn’t absorb
SNS, AII, Aldo, and ADH decrease
ANP increases in CD
changes in ____ will release ADH directly from ______
osmolality, posterior lobe of pituitary gland
changes in ______ reflect water balance
plasma Na
(+) H2O balance - 3 ways to describe it
input > output ….. low plasma[Na]….hyponatremic
(-) H2O balance - 3 ways to describe it
output > input ….high plasma[Na]….hypernatremic
most important osmoles in ECF:
most important osmoles in ICF:
ECF: Na+
ICF: K+
Na is an (ineffective/effective) osmole, meaning….
effective. doesn’t pass through membrane easily, sets gradient for water
ineffective: urea and glucose
What happens to the following (increase/decrease) when you drink a lot of water:
- Posm
- Osmoreceptors
- ADH secretion
- Thirst + H20 intake
- Water Excretion
- net effect on Posm
- Posm decreases
- osmoreceptors swell
- ADH secretion decreases
- thirst and H20 uptake decreases
- water excretion increases
- Posm increases
What happens to the following (increase/decrease) you eat a salty bag of chips
- Posm
- Osmoreceptors
- ADH secretion
- Thirst + H20 intake
- Water Excretion
- net effect on Posm
- Posm increases
- osmoreceptors shrink (water moves from inside cell to outside)
- ADH secretion increases
- thirst/H2O intake increases
- water excretion decreases
- Posm decreases
What are 3 main factors regulating ADH secretion
- Body fluid osmolality (Posm)
- Change in effective circulating volume (non-osmotic)
- Non-physiologic factors (pain, nausea, drugs)
change in ECV has a (more/less) sensitive response for ADH release
less sensitive-goes all out when reaches threshold
Which is more important in causing ADH release?
Non-osmotic change change in ECV–most important factor-survival mechanism
As change in ECV becomes more negative (decreases), ADH (increases/decreases)
ADH increases exponentially
ECV depletion vs. dehydration
ECV depletion: water AND sodium depletion
dehydration: ONLY water depletion
When urine flow rate (V) is low, urine osmolality is (low/high)
high (little amount, very concentrated)
when ADH is low, amount of urine is (low/high)
high, since ADH is responsible for water absorption.
While urine flow rate (V) and urine osmolality are inversely exponentially proportional, what factor stays constant?
Solute excretion (predominantly Na) excretion rate: Uoxm x V
Kidney can regulate solute excretion independently from what? What disease causes problems with this?
independently from water intake. renal disease disrupts this
Kidney can regulate solute excretion independently of water intake. Where does this occur in the nephron and explain the mechanism.
Principal cell of CD is where this regulation occurs. ADH binds to V2 receptors on basolateral side, causes addition of AQP channels on apical side, allows for H2O reabsorption.
Dilute urine:
Urine osmolality > Plasma Osmolality
Posm > Uosm (Uosm min = 50 mOsm/L)
Concentrated urine:
Urine osmolality > Plasma osmolality
Uosm > Posm (Uosm max = 1200 mOsm/L)
+ADH
What determines Uosm?
Water balance
Reference Posm
~300 mOsm/Kg H20
Diluting segments of the nephron and why
Thick ascending limb & distal tubule
water impermeable region of nephron
3 factors for max excretion (max dilute urine)
disease entities correspond to these
- in tact tubules (diluting segments)
- adequate delivery of H2O and solute (GFR)
- need absence of ADH
5 important factors for max reabsorption (max concentrated urine)
- in tact tubules (need TAL to establish a gradient by actively transporting NaCl out of lumen)
- adequate delivery of H2O and solute
- hyperosmotic medullary gradient (gradient set-up for water to be reabsorbed)
- need ADH–signal to tell principal cells to integrate AQP channels
- proper cell response to ADh signal
Diuretics have direct impact on which part of the nephron?
on the diluting segment, blocking NaCl reabsorption
