Kidney: Na+ (sodium) handling Flashcards
Filtered sodium is reabsorbed at all segments except
Descending limb of loop of henle
mention the distribution of Na+ reabsorption throughout segments
- Proximal tubule (PCT): 65% (main sodium reabsorption site)
- Loop of henle (ascending limb only) & early distal tubule: 25%
- late distal tubule & collecting duct: 10%
Describe reabsorption of Na+ at proximal convoluted tubule
first half= early PCT, reabsorbed by:
* Co transport with all filtered glucose & amino acids ‘
* Co transport with sulphate,PO4 & organic acids
* Responsible for reabsorption of 85-90% bicarb (HCO3)
* Counter transport with H+ (via Na+ H+ exchanger)
Late half of PCT, Na+ is reabsorbed by:
* reabsorbed with Cl- (passive diffusion)
Describe Reabsorption of Na+ at Thin descending limb of loop of henle
No reabsorption of Na+ due to absence of Na+ channels
Describe Na+ reabsorption at thin part Ascending limb of loop of henle
(like late PCT), passive reabsorption of Na+ with Cl- (NaCl), with impermiability to water, so Tubular osmolarity (solute conc.) decreases
Describe Na+ reabsorption at thick part Ascending limb of loop of henle
Reabsorption of 25% of filtered Na+ by Co transport with 1K+ & 2Cl- for each Na+
- with most of the K+ entering the cell being refluxed back into lumen via K+ leak channels
Explain why at Thick part Ascending limb of LoH, most K+ reabsorbed is refluxed back into lumen
- Ensure sufficent K+ concentration for optimum function of Cotransporter
- Keep Positive net potential inside the lumen, therefore facilitation paracellular reabsorption of Cations such as Ca++, Mg++, Na+
Via K+ Leak Channels
Causes of Bartter’s Syndrome
Defect in the Na+-K+-2Cl- co transporter, resulting in impaired reabsorption of sodium, potassium & Cl-
Manifestations/ results of Bartter’s Syndrome
- Hypokalemia
- salt wasting
- Volume depletion
- Hypocalcemia
- Hypercalcinuria
- Metabolic Alkalosis
Describe Na+ reabsoprtion at Early Distal Convoluted tubule
(like thick part ascending limb of LoH)
* Reabsorption of NaCl by Na+ Cl- Cotransporter, but impermiable to water
Diluting segment is made up of
- Ascending limb (of loop of henle)
- Early part Distal convoluted tubule
Describe Na+ reabsorption at late distal tubule & collecting duct
Fine adjustments under hormonal regulation (mainly aldosterone)
* by Principal (P) cells, reabsorbing 10% of filtered sodium in exchange with K+ secretion
Effect, Mechanism, site & importance of increasing GFR/ glomerulo-tubular balance on Na+ reabsorption (in isolated kidney independent on hormones
- Effect: increase in flow, increase in filtered Na+, increase in Reabsobed Na+, slight increase in Excreted Na+
- Mechanism: (in isolated kidney independent of Hormones) Renal tubules reabsorb constant percentage of filtered Na+ instead of Constant amount of Na+ (65%)
- Importance: preventing Overloading of Distal Convuluted tubule when GFR increases, &prevents inappropriate loss of Na+ and water when GFR increases
- Site: PCT, Loop of henle
Descibe effect of changing tubular flow rate on Na+ reabsorption
Slow flow Rate (decrease in GFR): Increases Reabsorption of Na+
Describe the effect of Increase in ABP on Na+ reabsorption, & mechanism of that effect
Increase in ABP increases Na+ & H2O Excretion (decreases Na+ reabsorption), by Compensatory mechanism independent of hormones or NS:
1. Increase in ABP causes Decrease in Angiotensin II secretion (most powerful Na+ retainer), so Na+ reabsorption decreases
2. Increase in ABP increases Hydrostatic pressure in peritubular Capillaries which increases ISF hydrostatic pressure, opposing Na+ reabsorption, causing Decrease in Na+ and H2O reabsorption
