Session 4 Flashcards
What is volume of water in the ECF dependent on?
What is ECF?
NA+
Plasma volume
How does the SGLT2 transporter work?
2 things in lumen compensate for loss of glucose therefore increasing in conc in the lumen, what are they?
What follows NA moving through?
Tubular cells transport 3na into ECF for 2K via active transport (3na-2K-atpase) on the basolateral membrane creating a low NA conc in the tubular cells. This drives the SGLT2 co transport of 3na and 1 glucose on apical membrane from lumen of PCT into tubular cells. The high levels of glucose mean it moves by facilitated diffusion into the capillary. The same happens with AA’s.
Cl and urea
Aquaporins
What does amiloride do in the PCT?
What about in DCT?
It inhibits NHE antiporter, so NA in for H out can’t happen. So it’s a diuretic as more NA thus water is in the lumen.
ENAC
In S2/3 of PCT how does CL move in and what result?
Another route of CL NA and h20 into ECF?
Still secondary active transport, the NA h antiport with NA coming in. This conc is then used for a CL NA antiport to bring CL into tubular cells on the apical membrane which then cotransport with k on the basolateral membrane to move into capillaries. This increases the number of osmoles thus bringing in water.
Through tight junctions
Main role of PCT and how?
% filtrate lost at glomerulus?
Main force driving water uptake?
What stimulates PCT reabsorption?
What does aldosterone target?
Reabsorbed 100% of glucose and AA’s via secondary AT and a lot of water due to it being highly water permeable.
20%
Hydrostatic pressure?
CD and DCT
RAAS
What happens to the PCT when renal artery BP increases?
Reduced NA h antiporter and reduced 3na-2K-atpase. So less NA thus h2o reabsorption. Thus increase sodium excretion (pressure naturiesis) and increase water excretion (pressure diuresis)
Cell type in PCT?
In loop of henle and relevance?
Concentration from cortex to papilla is?
Why is this relevant?
What happens in thin ascending limb?
Simple cuboidal
Squamous thus no solute transport.
Increasing.
In the descending limb water uptake due to this increase in concentration gradient. This concentrates NA in CL in lumen so they are ready for AT in ascending limb.
This gradient and the type of epithelium permits NA and CL passive uptake into capillaries.
What happens in the thick ascending limb?
3na2kaatpase leads NKCC2 (inhibited by furosemide) where NA k and 2 CL move in my cotransportation. KCLCT then moves CL and K into capillary. ROMK bring k back into lumen. So NA and CL again are reabsorbed.
Why is the ascending limb in LOH known as the diluting segment?
Descending limb absorbs h20 but not NaCl but the ascending absorbs NaCl but not H20. Therefore fluid leaving LOH is hypo-osmotic so more dilute.
What happens in DCT 1?
What inhibits NCCT?
What about in DCT2?
Hypo-osmotic solution is further diluted as secondary AT using NCCT where co-transport of NA and CL.
Thiazides.
ENAC (sensitive to amiloride) brings NA in so further dilution.
What happens to Ca in the DCT
Ca moves in to tubular cells, binds to calbindin is shuttled to the basolateral membrane and NCX exchanger takes place with 3 NA out of capillary for one ca.
Two regions of collecting duct?
Cortical- principal cells and intercalated cells
Medullary
What happens in principal cells?
Intercalated cells?
Secondary AT where NA reabsorption by ENAC. Now negative lumen provides driving force for CL- paracellular route uptake.ROMK excretes k and water in via aquaporins.
Aic secrete h and BIC secrete hco3.
Aic-h atpase and hkatpase
BIC use clhco3 antiporter
