Control of Plasma Volume Flashcards
Name how sodium can exit the body
Urine, faeces, sweat
Explain S1 sodium reabsorption in proximal tubule
- Apical membrane has Na-H exchanger, co-transport with glucose (sodium glucose co-transporter 2), co-transport with AA, co-transport with phosphate
- Basolateral membrane has Na/K ATPase which pumps 3 sodium ions out into interstitial space
- Aquaporins present to allow water to follow
- Concentration gradient of chlorine establishing which will aid passive reabsorption in S2-S3
Explain S2-S3 reabsorption in proximal tubule
- Apical membrane absorbs sodium via Na-H exchanger
- Paracellular chlorine absorbed from lumen due to concentration gradient created in S1 - more negative due to sodium reabsorption
- Transcellular chloride movement as well
- Aquaporins present
- Basolateral membrane has Na/K ATPase and chlorine channels
Explain sodium and chloride uptake in late proximal tubule
- Passive diffusion through tight junctions (paracellular reabsorption)
- High chlorine reabsorption as HCO3- levels decrease and Na is reabsorbed
Explain how PCT reabsorption into peritubular capillary occurs
- Proximal tubule highly water permeable
- Bulk transport or obligatory water reabsorption
- Reabsorption is isosmotic with plasma
- Driving force
- Osmotic gradient established by solute absorption - osmolarity in interstitial spaces higher
- Hydrostatic force in interstitium higher
- Higher oncotic force in peritubular capillary as proteins remain in efferent arteriole
Describe glomerulotubular (GT) balance and the effect of ECF volume (pressure natriuresis and diuresis)
- When renal artery blood pressure increases, causes reduction in sodium and therefore water reabsorption in proximal tubule
- Could be caused by reduced number of Na-H antiporter and reduced Na/K ATPase activity in proximal tubule
- Leads to increased sodium excretion (pressure natriuresis) and increased water excretion (pressure diuresis)
- ECF volume decreased and initial blood pressure rise diminished
Explain the difference in structure of the ascending and descending limb
- Descending limb have thin, flat cells with no mitochondria
- No brush border
- Aquaporins present to allow water movement
- Loose junctions
- Ascending limb have thicker cells with mitochondria present
- No aquaporins
- Solute movement occurs through active transport
- Tight junctions
Outline the action of water reabsorption in the descending limb
- Increasing concentrations of sodium further into medulla allow paracellular reabsorption of water through aquaporins in the loose junctions
- This concentrates the sodium and chloride ions in the lumen ready for active transport in the ascending limb
Explain the action within thin ascending limb
- Sodium ion reabsorption passive in thin ascending limb
- Due to concentration gradient created from descending limb
- Epithelium in thin ascending limb permits passive reabsorption by paracellular route
Explain the processes occuring in the thick ascending limb
- Apical membrane has NKCC2 transporter (sodium-potassium-chloride transporter) - active transport
- Sodium ions move into interstitium due to actions of Na/K ATPase
- Sodium moves into the cell via NKCC2 and then through Na/K ATPase (transcellular)
- High concentrations of sodium in nephron also allow paracellular reabsorption
- Potassium ions diffuse via ROMK (renal outer medullar potassium channel) back into lumen
- In the filtrate, there is less potassium ions so in order to maintain activity of NKCC2 transporter, potassium diffuses back into the filtrate
- Chloride ions move into interstitium through NKCC2 and paracellular diffusion
- This region uses more energy than any other in the nephron and is particular sensitive to hypoxia - very metabolic active
Describe sodium ion uptake in the early distal tubule
- Hypo-osmotic fluid enters
- Active transport of sodium through Na/K ATPase allows NCC (sodium chloride symporter) to reabsorb sodium from the lumen
- NCC sensitive to thiazide diuretics
Water permeability is fairly low
- NCC sensitive to thiazide diuretics
Describe sodium ion uptake in the late distal tubule
- Na enters by NCC and ENaC and leaves through Na/K ATPase
- ENaC sensitive to amiloride diuretics
- Movement through ENaC not electroneutral and difference drives paracellular chloride ion reuptake
Outline how calcium reabsorption occurs in DCT
- Apical calcium transport
- Cytosolic calcium immediately bound by calbindin, which shuttles calcium to basolateral aspect of DCT cell
- Transported out by NCX (sodium calcium exchanger)
- Tightly regulated by hormones such as parathyroid hormone and 1,25-dihydroxyvitamin D
Outline how sodium reuptake in principal cells occurs
- Principal cells (70%) allows reabsorption of sodium ions via ENaC on apical membrane
- Na/K ATPase on basolateral membrane driving force
- Transport of only sodium without chlorine produces a driving force for chloride uptake via paracellular route
Outline the role of intercalated cells
- Play an important role in acidosis and alkalosis
- Acid-secreting type A-IC
- Have H-ATPase and H/K ATPase on apical membrane
- Have Cl/HCO3 exchanger at basolateral membrane
- Bicarbonate-secreting type B-IC
- Allows active reabsorption of chloride ions