Water Balance Flashcards
Two key stimuli for increased ADH secretion?
- increased plasma osmolarity (more sensitive)
2. blood volume depletion
Secondary stimuli for ADH secretion:
pain
nausea
drugs (narcotics in particular)
Pathway for ADH secretion with increased plasma osmolarity:
Brain osmoreceptors depolarize –>
stimulates supraoptic nuclei in hypothalamus –>
Neurosecretory cells in posterior pituitary secrete ADH
**thirst is also stimulated
Pathway for ADH secretion by decreased plasma volume:
low MAP –> carotid and atrial baroreceptors –>
parasympathetic stim of hypothalamus paraventricular nuclei –> neurosecretory cells in post pituitary –> increased ADH secretion
Only nephrons that control water:
juxtamedullary (loops dive way down into medulla, glom still in cortex)
Variability of water reabsorption by percent?
80-99.5%
With full ADH effect, how much water gets excreted?
0.5%…..
With NO ADH effect, how much water can be excreted?
20%…36 L
Water % reabsorbed in prox tubule?
65%
Water % reabsorbed in descending LoH?
10% (vs 20% NaCl)
What joins NaCl in the interstitium around the lower loop of henle to increase osmolarity when ADH is in effect?
urea
Go learn about urea in lecture notes.
Not very flashcardable.
ADH deficiency?
Diabetes insipidus
If diabetes insipidus corrects with exogenous ADH the it’s called?
Neurogenic
don’t make ADH
If diabetes insipidus does not correct with exogenous ADH, then it is called?
Nephrogenic
kidney doesn’t respond to ADH (mutation of V2 receptor)
ADH receptor that stimulates transcription of aquaporins that get stored in intracellular vesicles for release to membrane?
V2
Player in the V2 receptor signaling pathway:
ATP
cAMP
Protein kinase A
cAMP response element binding protein (CREB)
CREB-P – the transcription factor
AQP2 inserts where?
luminal membrane (collecting tubule)
AQP 3&4 insert where?
basolateral membrane
Drug that can cause diabetes insipidus?
lithium
V2 receptor antagonist used in HF?
tolvaptan
Most important aquaporin?
2 (luminal)
If you don’t eat any protein or solutes, what happens?
No gradient formation in deep medullary region
no ability to resorb water because no urea or NaCl
“tea and toast”
“beer potomania”
Location of UT1?
distal third of collecting tubule
Location of UT2?
ascending LOH
UT1/2 upregulated by?
ADH