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
Enumerate Hormones which increase Na+ reabsorption
- Aldosterone (mineralocorticoid)
- Glucocorticoid
- Sex hormones
- Angiotensin II (most powerful)
Mechanism of Aldosterone on Na+ reabsorption
Facilitates Na+ reabsorption by:
* Acts on principal (P) cells at DCT & CD
* increases Na+ K+ ATPase pumps at basolateral border
* Increases Na+ channels at Apical (luminal) border
therefore Increases Na+ reabsorption in exchange of K+ or H+
Mechanism of glucocorticoid on Na+ reabsorption
weak Mineralocorticoid with same effect as Aldosterone
Mechanism of Angiotensin II on Na+ reabsorption
Facilitates Na+ reabsorption by:
1. Facilitates Aldosterone secretion
2. Direct effect on PCT (increase Na+K+ATPase & Na+-H+ Counter transporter)
3. VC of efferent arterioles, thus decreasing hydrostatic Pressure of peritubular capillaries (opposing Na+ reabsorption) & Increasing Osmotic pressure of Peritubular Capillaries (Favouring Na+ reabsorption)
Enumerate hormones decreasing Na+ concentration
- ANP (Atrial natriuretic peptide)
- PGE2
- Endothelin
Natriuretic: facilitates Na+ Secretion in Urine (decrease reabsorption)
Mechanism of ANP on inhibiting Na+ reabsorption
inhibits Na+ Reabsorption by:
1. Vasodilatation of Afferent Arteriole
2. Relaxation of Mesengial cells, leading to increased surface area
Causing Increase In GFR, filtered Na+ & Excreted Na+
- Inhibits Renin secretion, thus inhibiting Angiotensin II & Aldosterone Secretion
- Inhibits Na+K+ATPase & Na+ channels at Collecting Duct
Mechanism of PGE2 on inhibiting Na+ reabsorption
- inhibits Na+K+ATPase & Na+ channels
Mechanism of endothelin on inhibiting Na+ reabsorption
Increases PGE2
describe effect of Sympathetic Stimulation on Na+ reabsorption
It will Increase Na+ reabsorption & decrease Na+ excretion, by:
* Vasoconstriction of all renal vessels (Alpha 1 receptors), thus decreasing GFR
* increase Renin Secretion (Beta 1 recptors at Juxtaglomerular Apparatus), thus stimulating release of Angiotensin II & Aldosterone
* Direct action on renal tubule (alpha & beta receptors), increasing Na+ reabsorption
enumerate Diuretics affecting Na+ reabsorption & state their effect
- Carbonic Anhydrase inhibitor(Acetazolamide/diamox)
- Loop diuretic (lasix/furosemide)
- Thiazide
- Aldosterone inhibitor (aldactone)
all increase Na+ excretion (decrease reabsorption)
