k regulation

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  1. shift k out of cell to ecf
  2. k balance acheived by
    urinary excretion of k exactly=  intake on the diet
  3. k excretion can vary
    * from 1-100% of the filtered load

    • *depends on :
    •  dietary k intake 
    • aldosterone levels 
    • acid base status
  4. glomerular capillary
    filtrated freely across the glomerular capillary 

    TF/P(K) in bowmans space is 1 
  5. proximal tubule 
    reabsorbs 67% of the filtered K ,along with Na and  H2O
  6. thick ascending loop of henle 
    • 1.reabsorbs 20% 
    • 2. re-absorption is from the Na-k-2Cl cotransporter in the lumenal surface of the cells in thick ascending limb 

    • The side of the tissue facing the lumen is the apical surface of the epithelial tissue
  7. distal tubule and collecting duct
    • reabsorbs or secretes k
    • depending on dietary intake
  8. distal tubule and collecting duct REABSORB K
    1.H,K ATPase in the apical membarance of the INTERCALATED CELLS A .

    • 2.OCCURS ONLY on LOW K diet -k depletion
    • low intracellula k so that is driving force for k secretion decrease , the A intercalated cells are stimulated to reabsorb k by H-K-ATPase
    • 3.can be very low 1% of filtered load  because kidney conserves as much k as possible
  9. secretion o k
    occurs in in principal cell

    variable and accounts for the wide range of urinary k exrition 

    • depends on
    • 1.dietary k
    • 2.aldosterone levels 
    • 3.acid base status
    • 4.urinary flow
  10. mechanism of the distal k secretion in principal cells  
    • 1.basolateral membrane , k is actively transporte into the cell by: Na-k pump
    • this mechanism maintains a high intracellular k concentration 
    • 2.lumenal membrane  , k is passively transported into the lumen  (flow rate dependent ) through k channels 
    • the magnitude of the passive secretion is determined by the electrical and chemical driving forces on k across the luminal membrane 
    •  maneuvers which increase the intracellular k cc or decrease the luminal k cc will increase secretion by increasing the driving force

  11. factors change the distal k secretion 

    distal k secretion by the principale cells is increased by electrochemical driving force for k across the lumenal membrane is increased
    1. at high k diet (in which intracellular k increases) increase secretion 

    • 2.aldosterone ---> increase k secrition by 
    • increase # of luminal membrane k channels
    • (tfser bldftr ljded)

    • 3. acid base:isohydria and k homeostasis are coupled
    • effectively H/K antiport across the basolateral cell membrane 
    • alkalosis increases k secretion , blood contains too little H+ 
    • ACIDOSIS  DECREASE K SECRETION , blood cont. excess of H+

    • 4. thiazide and loop diuretics ---> increase K secretion 
    • diuretics increase flow rate through distal tubule (thiazidediuretics,loop diuretics) cause dilution of the luminal k concentration so increase k secretion. 
    • (leads to hyperkalemia)

    • 5.k spearing diuretics 
    • increase k secretion 
    • if used alone cause hyperkalemia 
    • 6.luminal anions: 
    • excess anions in the lumen cause an increae in k secretion by increasing the negativity of the lumen , which favors k secretion 
  12. increased distal k secretion
    • 1.high k diet
    • 2.hyperaldesteron
    • 3.luminal anions
    • 4.loop diuretics
    • 5.thiazide diuretics 
    • 6.alkalosis
  13. dicreased distal k secrition
    • 1.low k diet
    • 2.hypoaldesteron
    • 3.acidosis
    • 4.k sparing diuretica
  14. hormonal regulation of EC(EXTRA CELLULAR) K CONCENTRATION

    • 2.insulin:
    • *direct stimulation of NA-K PUMP
    • *STIMULATION OF NA-H antiporter in liver muscle and left tissue 

    3.katecholamines direct stimulation of Na-K pum
  15. calcium + phosphate house hold
    • regulation includes the function of
    • 1.parathyroid gland
    • 2.bones
    • 3.gastrointestenal glands 
    • 4.kidney
  16. ca/person
    1 kg
  17. phosphate/body
    700 g
  18. regulation of Ca household
    Ca2+ intake: 200-1000 mg/day, 5-25 mmol/day   40 - 50 % of the plasma Ca2+ content (2,2 - 2,6 mmol/L) is protein-bound.

    • This bound protein is not filtrating in the glomeruli,
    • The non-protein bound Ca2+ is freely filtrating
    • 97-99% of the filtrated Ca2+ is reabsorbed in the tubular system.

    The daily excretion is 2,5 - 7,5 mmol Ca2+.
  19. ca intake
    200-1000 mg/day

    5-25 mmol/day
  20. 40-50% plasma Ca content is protein bound
    2.2-2.6 mmol/L
  21. ca excretion daily
    2.5-7.5 mmol
  22. Calcium excretion through the kidney.
    1. 70 % of the filtrated Ca2+is reabsorbed in the proximal tubule

    2. 20-25% of the filtrated Ca2+is reabsorbed in the Henle-loop

    3. A 5-10 % of the filtrated Ca2+is reabsorbed by an ACTIVE PROCESS in the distal nephron 
  23. Ca and loop diuretics (Fe: furosemide)
    causes increased urinary Ca excretion 

    because Ca reabsorption is linked with Na reabSorption in LOOP OF HENLE
  24. increase the Ca reabsorption
    • 1.PTH - in distal tubule by activating adenylate cyclase
    • 2. thiazide diuretics in distal tubule so decrease Ca excretion
  25. phosphate reabsorption
    85-95 % of the filtrated phosphate is reabsorbed in the proximal tubuliby      Na-phosphate  cotransport

    due to the fact that the distal nephron does not reabsorb phosphate --> 15%of the remaining PHOSPHATE IS EXCRETED

    This reabsorption is coupled to Na+ reabsorption, thus it has a Tm value .
  26. phosphate excretion
    Regulation of phosphate excretion is achieved by parathyroid hormone- PTH that inhibits the phosphate reabsorption in the proximal tubuli.by ACTIVATING Adenylate Cyclase, generating cyclic AMP 

    High plasma level of PTH  may yield the excretion of 40 % of the filtrated amount (hyperphosphaturia).

    Low plasma level of PTH is associated with the excretion of less than the 5% of the filtrated amount (hypophosaturia).

    PTH acts through these mechanisms on the plasma Ca++ level. PTH acts through specific receptors on the baso-lateral surface through specific receptors through the route described at Ca++- ions.
    urinary buffer for the H excretion of h2po4
  28. Mg reabsorption
    • 1.proximal tubule
    • 2.thick ascending limb
    • 3.distal tubule
  29. Mg and Ca in the thick ascending limb 
    Mg and Ca compete for reabsorption in the thick ascending limb 

    hypercalemia-->increase in Mg excretion (by inhebiting Mg reabsorption)

    hypermagnesemia-> causes increase in Ca excretion (by ihebiting Ca reabsorption)
  30. hormonal regulation of calcium and phosphate
    calciotrop hormons:
  31. calciotrop hormones are: 3
    • 2.CALCITONIN-thyroid gland
  32. PTH
    • regulate [CA]SERUM
    • synthesized and secreted by the CHIEF CELLS of parathyroid glands
    • 48 amino acids
    • prephormon (145 amino acids)
  33. secretion of PTH
    regulated by the SERUM [Ca] binding to Ca sensing receptors in parathyroid ell membrane

    PTH 1.binds to PTH receptors 2.increase adenilate cyclase and phospholipase C activity

    PTH effect is executed by contribution of IP3 and cAMP

    • PTH INCREASE when  [Ca] decreased
  34. second messanger for PTH SECRETON IS BY PARATHYROID GLAND
    INCREASE PTH secretion
  36. PTH effect
    • 1.in kidney and bone DIRECT EFFECT
    • 2.small intestine indirect effect through calcitriol

  37. PTH function is
    • 1.increase Ca reabsorption in thick ascending limb  and the distal nephron
    • 2.phosphate excretion
Card Set:
k regulation
2013-11-25 00:09:31

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