what is vapopressin? what does it do?
vapopressin (aka ADH) inhibits diuresis by incr amt of water reabsorbed from filtrate
binds extracellularly, starting a second messenger cascade (GPCR)
so ADH is active and water is resorbed from filtrate. where does it go?
vasa recta (surrounding vasculature), which is really permeable to water
what is the “single effect?” how does it play into multiplication?
ok so we have the desc limb, asc limb, and int fluid in bw. we gotta remember the desc limb is permeable to everything, while the asc limb is permeable to salts but not water.
- Na+ moves out of desc limb via ACTIVE transport, increasing the int fluid osm
- because the asc limb is permeable to everything, it will reach eq w the int fluid. this means:
- salts move into the asc limb
- water moves out into int fluid - bc the desc and asc limb are connected, the fluid in the desc limb moves to the asc limb. then we rinse and repeat (multiplication)
what does ADH do again?
incr expression of aquaporins – water becomes more permeable and gets resorbed
what does the vasa recta do?
takes resorbed water and moves into circulation, incr blood pressure
we’ve seen that arid species have larger renal paps, while aquatic species have smaller renal paps. what does this imply for survival
renal paps are where loop of henle is held; larger renal paps indicate more water resorption, as seen in arid species, and the opposite for smaller renal paps and aq species.
what this tells us is that the renal pap + loop is an expensive structure (and we know this bc of the active transport req in single effect)
– animals don’t maintain if they dont need it (as seen in aq species)
explain what happens in the prox tube
prox tube is critical for ultrafiltration
- NaK pump makes Na scarce in the cell, making a favourable Na gradient
(not as important but there’s also passive K diffusion bc of the K+ buildup, either into the int fluid of tubular fluid) - Na/glucose cotransporter brings glucose across against its diffusion gradient
- glucose is brought into int fluid passively due to gradient
big takeaway! early prox tube job is to take in glucose and amino acids via cotransportation
what happens in the asc limb? what would happen if our asc limb were to stop working properly?
- same NaK pump shit as normal
- this time we use the NKCC pump, w K and 2 Cl against their gradients
- many things
- Cl- moves into the interstitial fluid due to gradient
- to match electronegativity, Na+ moves out paracellularly
- K passive moves into int fluid
thus we get [whats the purpose]
if the asc limb were to stop working, it would prob be in the NKCC transporter - the result would be that osmolarity couldn’t do its single effect thing, so water wouldn’t be able to move out from desc limb into int fluid –> no resportion
what is AQP-2? do we have proof it actually does anything?
when exposed to ADH, the collecting duct epithelial cells get flooded with aquaporin-2 (AQP-2) cells, incr water permeability
how is the octopus kidney system similar to a human’s? how does it differ?
similarities:
- vascular system interacts w renal system at the renal appendages (high in SA, similar to our [something idk])
- has ultrafiltration similar to our bowman’s, at the pericardial sac
differences:
- secretion before filtration (whereas we kinda do it together in one step)
compare a grasshopper’s kidneys to a human’s
- stellate cells control anion (passing?) similar to podocytes (filtration)
- malpigian tubules prod filtrate (secretion) kinda like in bowmans
- rectal pads are used for resorption, similar to loop of henle
- hindgut sel reabsorbs water and salts (where the rectal pads are)
if u feed insects pure water, what happens? conversely, if u feed them saltwater, what happens?
feed pure water:
- incr water intake means u have to retain salts
- salts will be taken back through rectal pads
feed salt water:
- incr salt intake means u have to retain water
- salts are secreted by the malpig tubes
