L3:tubular structure and function Flashcards
2 routes of transport for fluid moving from the tubule to the interstitial space
- paracellular route
- transcellular route
paracellular route=
between tight junctions, through lateral intercellular folds
transcelluler route=
across apical, basolateral and translateral surfaces
3 methods of transcellular transportation
- primary active transport
- secondary active transport
- ion channels
what is present on the apical membrane of cells to increase absorption
microvilli
how much reabsorption happens in the PCT
2/3rd of nearly all filtrate
how much glucose is reabsorbed in the PCT
100%
no glucose in urine
what happens to glucose handling in diabetes mellitus
plasma glucose exceeds tubular maximum so glucosuria
what is diabetes insipidus
problem with releasing ADH from pituitary gland, loss of salt and water
what glucose transporter is on the apical membrane in early PCT
SGLT2
what is SGLT2 affinity/capacity for glucose
high capacity
low affinity
what glucose transporter is on the basolateral surface in the early PCT
GLUT-2
apical glucose transporter in late PCT
SGTL-1
basolateral glucose transporter in late PCT
GLUT-1
SGLT-1 affinity/capacity for glucose
low capacity
high affinity
at what point is glucose excreted into filtrate not reabsorbed
when levels pass the tubular transport maximum
what effect does glycosuria have on urination
polyria and polydipsia (thirst)
how are AA reabsorbed
98% via transcellular route in PCT
how are AA filtered in the glomerulus
freely filtered
were are small peptides reabsorbed
all reabsorbed in PCT
how are small peptides reabsorbed
hydrolysed by brush border peptidases on apical membrane and reabsorbed as AA
what percentage of proteins enter the filtrate
1%
how are proteins reabsorbed
protein is endocytosed at apical membrane by peptide transporters
the peptide transporters for protein reabsorption
PepT1
PepT2
PepT1 capacity/ affinity=
high capacity
low affinity
PepT2 capacity/affinity
low capacity
high affinity
what happens to proteins in endosome
lysozymes join and hydrolyse protein into AA
2 secretions of the PCT
organic anions
organic cations
2 organic cations
creatinine
drugs
3 drug cations secreted in PCT
trimethoprim
cimetidine
quinidine
symporter=
substances go in same direction
antiporter=
substances go in opposite direction
amount of Na reabsorbed in PCT
70%
what percentage of Na+ is secreted per day
0.4%
main route of Na+ reabsorption
transcellular route
what pump drives Na+ into the interstitial space
Na-K-ATPase
how is Cl- reabsorbed
paracellularly driven by electrical gradient created by Na+ reabsorption
osmolarity of fluid in beginning of loop of henle
isotonic with plasma
as fluid descends down loop of henle what is the fluid movement
water moves out into interstitium
what happens to osmolarity of fluid in loop of henle as you move down
becomes hypertonic (osmolarity increases)
what substance movement happens in the ascending loop
Na/K/Cl actively pumps ion out of fluid into interstitium
osmolarity of fluid in ascending loop=
hypotonic
osmolarity of fluid in DCT
hypotonic
what pumps do loop diuretics effect
Na/Cl/K co-transporter decreasing ion transport moving into blood
e.g of loop diuretic
furosemide
in DCT what channels does Na move through on apical membrane
ENaC epithelial sodium channel
where do thiazides act
DCT
what pump do thiazides work on
Na/Cl/K
2 types of collecting ducts
cortical
medullary
what happens in principal cells of cortical
sodium reabsorption via ENaC on apical and potassium channels
what drug blocks ENaC
amiloride
2 Na+ retaining factors
- renin
- sympathetic nervous system
- vasopressin
Na+ losing factor
-atrial natriuretic peptid
what causes an increase in atrial natriuretic peptide release
increase in blood pressure
atrial natriuretic peptide effect=
inhibits reabsorption of sodium –> decreasing Bp
3 things that act on arterioles to lose Na+
- Dopamine
- Bradykinin
- prostaglandins
main site of Cl reabsorption
PCT -65%
% of Cl reabsorbed in TAL
25%
main site of magnesium reabsorption
thick ascending loop
how is Mg reabsorbed
paracellularly
what increases phosphate excretion
PTH
main site of phosphate reabsorption
PCT
what makes the collecting ducts more permeable to reabsorb water
ADH
what substance move out of the collecting duct into interstitium to maintain conc
urea
where is blood osmotic pressure detected
osmoreceptors in hypothalamus
what receptors does ADH work on
v2 receptors in cortical collecting ducts
where is aldosterone released from
zona glomerulosa in adrenal glands
what does aldosterone bind to
MR (mineralocorticoid receptor
3 things aldosterone-MR increases
- ENaC
- K+ channels on apical membrane
- increase in basolateral Na/K/ATPase pump
2 reasons aldosterone is released
Ang 2
increase K+ levels
2 K+ sparring diuretics
spironalactone
amiloride
