B5.040 Renal Physiology III: Regulation of Extracellular Fluid Volume and Osmolarity Flashcards
what is regulated to maintain ECF volume
Na+ intake and excretion
what is regulated to maintain ECF osmolarity
water intake and excretion
water balance in the body
2.4 L/day intake (2 L ingested, 0.4 L from metabolism)
loss of 2.4 L/day (1.5 L from kidney, 0.4 L from skin and lungs, and 0.1 L from intestine)
what controls water uptake
mechanism of thirst
what controls water elimination
reabsorption in the kidney
discuss the mechanisms involved when there is an increase in extracellular fluid osmolarity
rise in osmolarity > stimulated thirst center and osmoreceptors > water ingestion stimulated by thirst center > ADH production stimulated by osmoreceptors > ADH stimulates reabsorption of water from collecting duct > urine osmolarity increases and volume decreases
what portions of the nephron are the key players in water reabsorption
proximal tubule- automatic fashion
distal/collecting tubule- regulated by ADH
other name for ADH
AVP
arginine vasopressin
where is ADH synthesized
hypothalamus
discuss the relationship between plasma oncotic concentration and ADH release
linear relationship, a small variation in osmolality can cause immediate changes in ADH
basal ADH = 2ish
max effective concentration of ADH on kidneys = 4ish
pressure/volume changes effects on ADH release
decreases in pressure and volume both cause release of ADH
ADH is more sensitive to osmotic changes than to pressure/volume changes, however
general function of ADH
establishes a high water permeability at the distal and predominantly collecting tubules
causes water to be rapidly reabsorbed
urine volume diminishes and osmolarity increases
relationship between plasma ADH levels, urine osmolality and flow rate
low ADH = max flow, min osmolality
high ADH = min flow, max osmolality
mechanism of ADH in renal tubule
binds to V2 receptor on BM
activates cAMP and thus PKA
phosphorylation of aquaporin 2 molecules cause them to move to the membrane
once in membrane, aquaporins facilitate reabsorption of water from lumen
mechanism of ADH in vasculature
binds to V1 receptor on smooth muscle cell
stimulates Ca2+ entry into cell and release from sarcoplasmic reticulum in cell
increased Ca2+ conc increased actin-myosin coupling
vasoconstriction is triggered
discuss the countercurrent exchange mechanism of the loop of henle
descending loop: permeable to salt and water, water flows out and salt flows in to equilibrate with the medulla, generating an extremely hypertonic solution at the bottom of the loop
ascending loop: permeable to salt but NOT water, salt pumped out against gradient by NKCC yielding an extremely hypotonic solution at the top of the loop
discuss the effect of the countercurrent mechanism on the distal and collecting tubules
receive hypotonic solution from loop of henle
in presence of ADH, transport excess fluid out of tubule into ISF down the conc gradient into the salty medulla
descending loop of henle
concentrating segment
ascending loop of henle
diluting segment
discuss the vasa recta as a part of the countercurrent exchange mechanism
very slow rate of blood flow in a hairpin formation
allows blood to flow through cortex without disturbing osmotic gradient
both limbs of vasa recta permeable to salt and waterr
recycling of urea as a part of the countercurrent exchanger
urea concentrated in medullary ISF and in the tubular fluid
inner medullary collecting duct is permeable to urea and there is a gradient for passive diffusion of urea into medullary ISF
urea then diffuses from ISF into vasa recta
as vasa recta ascends, urea diffuses back into the ISF and then back into the descending capillary
primary engine of the countercurrent mechanism
reabsorption of salt without water by the thick ascending limb of the loop of henle
where are salt and urea trapped and why
medulla
countercurrent flow arrangement traps them while minimizing the water that enters
establishes a gradient to be capitalized on by the collecting tubule when ADH is present
factors affecting the kidney’s ability to concentrate the urine
- length of loops of henle (modifies vertical osmotic gradient)
- ADH levels that control water permeability in the collecting tubule
- blood flow rate through the medullary capillaries (when increased, more salt is reabsorbed from the interstitium and countercurrent effect decreases)
- factors that influence concentration of urea, higher urea in medulla favors countercurrent mechanism
- drugs and diuretics that affect salt reabsorption in the loop of henle inhibit countercurrent effect
describe the process of water diuresis
excess water ingested (polydipsia) > decreased extracellular fluid osmolarity > decreased ADH secretion > decreased permeability of distal nephron to water reabsorption > solute reabsorption continues > increased urine dilution
diabetes insipidus
defect in ADH-dependent water reabsorption
max water excretion
20 L/day
11% of GFR
polyuria
> 3 L of water per day
describe the process of solute diuresis
excess solutes in the filtrate > decreased water reabsorption in the proximal tubule > partial, but insufficient compensation by distal tubule reabsorption > urine osmolarity isotonic or close to plasma > increased urine volume
why might there be excess solutes in the filtrate
due to presence of osmolites
inhibition of salt reabsorption by diuretics
response to: loss of water > solutes
water reabsorption
urine volume decreases
urine concentration increases
response to: excess water over solutes
water excretion
urine volume increases
urine concentration decreases
response to: excess of isotonic fluid
water and solute excretion
urine volume increases
urine concentration isotonic
range of urine osmolarity
50-1200 mOsmole/kg H2O
range of urine volume
0.5 to 20 L
which 4 parallel effector pathways are stimulated by changes in effective circulating volume
- renin-angiotensin system
- sympathetic nervous system
- ADH
- ANP
these all act on the kidney to change reabsorption of salt or modify renal hemodynamics
ADH actions at low vs high levels
levels under 5 = major effect on tubular water absorption
levels above 5 = have reached maximum effect on kidneys, exert additional effect by causing vasoconstriction of arterioles
4 primary natriuretic peptides, their location, and their stimulus for release
ANP - atria - increased heart volume
BNP - ventricle - increased heart volume
CNP - brain - increased intravascular volume
urodilatin - kidney- increased volume and Na+ load
mechanism of action of NPs on vascular cells
opposite of ADH
caused vasodilation
mechanism of action of NPs on collecting duct cells
inhibit Na+ reabsorption by down regulating ENac channel
how do NPs differ from the other 4 mechanisms involved in volume regulation
only mechanism that products from TOO MUCH volume, all others worried about too little volume
effect of NPs on juxtaglomerular apparatus
increased blood volume > increased ANP released from atria > afferent arteriole vasodilation > increased GFR > increased Na+ load to macula densa > decreased renin release > increased salt and water excretion, decreased BP
effects of NPs on adrenal corext
decrease aldosterone to increase salt and water excretion and decrease BP
if u don’t know the renin-angiotensin-aldosterone system yet r u even TRYING
ugh idk i just really don’t want to type it out again
what is the ~new~ function of angiotensin II tho
stimulates ADH release to stimulate water reabsorption in collecting duct
stimuli of increased renin release
decreased BP
decreased Na+ delivery to macula dense
increased sympathetic activity
how does sympathetic nerve activity influence blood volume
decreased atrial volume > stimulates sympathetic nerve activity > acts on renin angiotensin system BUT also directly stimulates tubular reabsorption via a receptors
effects of all pathways to an increased filling volume in the atria
- decreased ADH
- increased ANP
- decreased renin secretion
- decreased sympathetic discharge
INCREASE SALT AND WATER EXCRETION
sensors of ECF volume
baroreceptors
volume receptors
sensors of ECF osmolarity
hypothalamic osmoreceptors
effector pathways of ECF volume regulation
ADH
ANP
renin-angiotensin-aldosterone
sympathetic nerves
effector pathways of ECF osmolarity
ADH
thirst
effects of regulatory pathways on ECF volume
short term: heart, vessels
long term: kidneys
effects of regulatory pathways on ECF osmolarity
kidney brain (water intake)
what is regulated for ECF volume
short term: BP
long term: Na+ excretion
what is regulated for ECF osmolarity
renal water excretion
water intake
