pumps and ATPases Flashcards
what are the 2 methods of transport across the membrane?
diffusion or active transport
types of diffusion
simple and facilitated
why do things get transported by facilitated transport?
ionic
hydrophilic
polar
too large
active transport
moving against a concentration or electrochemical gradient
what is kidney important for?
regulating fluid waste vitamins minerals hormones electrolytes
where is the Na+/K+ pump/ ATPase
every epithelial of the kidney
only on the interstitial side of cell (basolateral membrane)
most cells do
what does the Na+/K+ pump do?
3 sodium bind
phosphorylating it
releasing sodium to other side and allows binding of 2 potassiums against the concentration gradient
secondary active transport
allowed by the Na+/K+ pump by passive entry, anti-porter and co-transport
anti-porter
diffuses sodium into cell and exchanges for H+
no energy used
co-tranport
Na+ and another solute diffuse into cell
e.g. glucose simporter
nephron can
dissociate the reabsorption of water and sodium
where is most sodium reabsorbed?
PCT
50%
nitrogen/ hydrogen exchanger
sodium reabsorption in ascending loop of Henle
sodium/ potassium/ chloride transporter
water in loop of henle
ascending = water impermeable descending = water permeable
sodium reabsorption in DCT
fine-tuning
by Na+/Cl- transporter
ENaC
what happens if K+ levels increase
aldosterone released by RAAS
affects principal cells in collecting duct
causes production of more sodium potassium pumps and ENaCs
regulation of transporters
transporters are continuously recycled
transporter synthesis can be up-regulated or
degradation inhibited degradation can be up-regulated
to adjust electrolyte concentrations
daily recommendation for K+
3500mg
what amount of K+ causes adverse effects?
6000mg, but no upper limit
Liddle’s syndrome
gain of function due to impaired degradation of ENaC in collecting duct
pseudohyperaldosteronism
low renin and low aldosterone (only looks like aldosterone is up)
Na+ retention
increased ECF volume and BP
decreased K+
how to treat Liddle’s syndrome
low sodium diet
diuretic
Gitelman’s syndrome
Na+/Cl- transporter loss of function
Bartter’s syndrome
sodium/potassium/ 2 chloride transporter loss of function
Pseudohypoaldosteronism
loss of function of ENaC
low sodium
serum osmolality is high because another solute replaces sodium
primary polydipsia
drinking in excess causing hyponatraemia
low serum sodium, serum osmolality and urine osmolality
what decreases aldosterone
increased water
where does reabsorption of water by ADH take place?
collecting duct
ADH
increases the permeability of the collecting ducts to water
different types of aquaporins are there in the nephron?
1,2,3,4,6,7,8,11
allows dissociation of water and sodium transport
what do aquaporins do?
control osmolality
how does ADH increase permeability of the collecting duct?
binds to receptors on interstitial side of epithelial cells
GPCR activates adenyl cyclase to convert ATP to cAMP which activates PK A causing vesicle containing AQP2 to move and insert into the membrane on the luminal side
AQP3&4
ready in cytosol to be expressed on interstitial side
open channels for reabsorption of water
what transporter reabsorbs glucose?
GLUT2 on PCT
facilitated by Na+/K+ pump
loop diuretic
blocks NKCC
loss of NaCl and K+
reabsorb less K+ so decreases osmotic gradient
less water can be reabsorbed due to reduced osmolality in interstitial fluid
increases Na+ in collecting duct, so absorbed by ENaC causing more K+ lost
changes membrane potential so Ca2+ and Mg2+ lost
loss of fluid activates aldosterone via RAAS increasing ENaC activity
NKCC
sodium/ potassium/ 2 chloride cotransporter
end result of loop diuretics
loss of Na+ and water
hypokalemic metabolic acidosis
increased Ca2+ loss
