Lecture 4 - Reabsorption Along the Tubule Flashcards
How is glucose reabsorbed in the DCT?
- Virtually all glucose reabsorbed in PCT
- Via secondary active transport, driven by Na+ concentration gradient created by Na/K ATPase
- Glucose moves into cell coupled with Na+ via SGLT1/2, moves into blood via GLUT channels down concentration gradient.
Why does glycosuria occur during during diabetes and in pregnancy?
- High blood glucose, Tm is reached (maximum tubular resorptive capacity)
- Glucose not fully reabsorbed, lost in urine (glyoscuria)
- Tm for glucose falls in pregnancy, glucose excreted in urine
How are AA’s reabsorbed in the PCT?
- Via secondary active transport (similar to glucose)
- Symported with Na+, using concentration gradient provided by Na/K ATPase
- Tm limited process
How are bicarbonate ions reabsorbed in the PCT?
- HCO3- & H+ ions combined to form carbonic acid (H2CO3)
- Carbonic acid broken down into H20 & CO2 via carbonic anhydrase
- CO2 freely diffuses into the cell, recombined with H2O to form carbonic acid via carbonic anhydrase
- Carbonic acid broken back down into HCO3- & H+
- HCO3- moves into blood via HCO3-/Na+ co-transporter
Therefore, give a summary of all the channels involved in the PCT
- Na+ symporters for glucose, AA’s + peptides
- H2O channels
- Na/H exchanger (providing H+ ions for combination with HCO3-)
- Na/K ATPase
- Cl- ion channel
- HCO3-/Na co-transporter
- Cl-, Mg2+ + H2O solvent drag through tight junction
How does concentration gradient change from the cortex into the medulla?
Where in the LoH is water reabsorbed & where is it not reabsorbed?
- Increasing concentration gradient from cortex to papilla
- Water reabsorbed in thin descending limb, ascending limb impermeable to water
How are Na+, K+ & Cl- ions reabsorbed in the thick ascending limb of the loop of henle?
How are Mg2+ & Ca2+ ions reabsorbed in the TAL of the LoH?
- Concentration gradient set up by NaK2Cl co-transporter on apical membrane
- ROM-K channel on apical membrane removes some K+ to keep K+ moving in via co-transporter
- K+Cl- ions reabsorbed through K/Cl co-transporter
- Another Cl- ion channel for reabsorption
- Na/K ATPase on basolateral membrane removes Na+
- Mg + Ca ions reabsorbed via paracellular transport due to electrical gradient set up by Na/K ATPase
What are the principles of reabsorption in the PCT?
- Reabsorption is isosmotic
- PCT responsible for bulk reabsorption of many solutes
- Very metabolically active, high concentration of mitochondria
- Provides energy for Na/K ATPase
How are Na+, Cl- and Ca2+ ions reabsorbed in the DCT?
- Na/K ATPase creates concentration gradient for Na+ to move in via ENaC and via NaCl co-transporter.
- Ca2+ moves in via Ca2+ channel, exits via NaCa antiporter
- Also single channels for K+ and Cl- ions
How is Na+ reabsorbed in the principal cells of the collecting duct?
How is water reabsorbed in principal cells of the collecting duct?
- Na/K ATPase on basolateral membrane and removal of K+ through ROMK channel provides concentration gradient for secondary active transport of Na+ through ENaC - Aldosterone causes increase in ENaC expression so increase in Na+ reabsorption.
- ADH causes AQP channel expression after binding to V2 receptors, allows for reabsorption of water.
What diuretics work in the PCT?
What diuretics work in the TAL of the LoH?
PCT:
- Carbonic anhydrase inhibitors (diuretic) - preventing HCO3- reabsorption
- Amiloride - blocks Na/H exchanger
TAL:
- Loop diuretics - block NaK2Cl co-transporter
What diuretics works in the DCT?
What diuretics work in the CD?
DCT:
- Amiloride - blocks ENaC
- Thiazides block NaCl co-transporter
CD:
- K+ sparing diuretics - block aldosterone, so no increase in ROM-K channels or ENaC
What is central and nephrogenic diabetes insipidus and how are they treated?
Central:
- Impaired ADH synthesis or secretion by hypothalamus, e.g.: by brain injury, tumour, aneurysm etc.
- Water inadequately reabsorbed from CD’s, so large quantities of dilute urine produced
- Treated by synthetic ADH (desmopressin)
Nephrogenic:
- Acquired insensitivity of kidney to ADH
- Water not reabsorbed, large quantities of dilute urine produced
- Low salt/Low protein diet, no current treatment to correct deficit
What is syndrome of inappropriate antidiuretic hormone secretion (SIADH)?
What are the consequences?
- Excessive release of ADH from posterior pituitary gland or another source
- Dilutional hyponatreamia, total body fluid increased
Give a summary of what % of total Na+ and H2O is reabsorbed in each section of the nephron?
Kewl
