-
shift k out of cell to ecf
hyprkalemia
-
k balance acheived by
urinary excretion of k exactly= intake on the diet
-
k excretion can vary
* from 1-100% of the filtered load
- *depends on :
- dietary k intake
- aldosterone levels
- acid base status
-
glomerular capillary
filtrated freely across the glomerular capillary
TF/P(K) in bowmans space is 1
-
proximal tubule
reabsorbs 67% of the filtered K ,along with Na and H2O
-
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
-
distal tubule and collecting duct
- reabsorbs or secretes k
- depending on dietary intake
-
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
-
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
-
mechanism of the distal k secretion in principal cells
- 1.basolateral membrane , k is actively transported 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
-
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
-
increased distal k secretion
- 1.high k diet
- 2.hyperaldesteron
- 3.luminal anions
- 4.loop diuretics
- 5.thiazide diuretics
- 6.alkalosis
-
dicreased distal k secrition
- 1.low k diet
- 2.hypoaldesteron
- 3.acidosis
- 4.k sparing diuretica
-
hormonal regulation of EC(EXTRA CELLULAR) K CONCENTRATION
1.ALDOSTERON
- 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
-
calcium + phosphate house hold
- regulation includes the function of
- 1.parathyroid gland
- 2.bones
- 3.gastrointestenal glands
- 4.kidney
-
-
-
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+.
-
ca intake
200-1000 mg/day
5-25 mmol/day
-
40-50% plasma Ca content is protein bound
2.2-2.6 mmol/L
-
ca excretion daily
2.5-7.5 mmol
-
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
-
Ca and loop diuretics (Fe: furosemide)
causes increased urinary Ca excretion
because Ca reabsorption is linked with Na reabSorption in LOOP OF HENLE
-
increase the Ca reabsorption
- 1.PTH - in distal tubule by activating adenylate cyclase
- 2. thiazide diuretics in distal tubule so decrease Ca excretion
-
phosphate reabsorption
85-95 % of the filtrated phosphate is reabsorbed in the proximal tubuli. by 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 .
-
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.
-
PHOSPHATE
urinary buffer for the H excretion of h2po4
-
Mg reabsorption
- 1.proximal tubule
- 2.thick ascending limb
- 3.distal tubule
-
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)
-
hormonal regulation of calcium and phosphate
calciotrop hormons:
-
calciotrop hormones are: 3
- 1.PTH-PARATHYROID GLAND
- 2.CALCITONIN-thyroid gland
- 3.VITAMIN D-CALCITORIOL
-
PTH
- regulate [CA]SERUM
- synthesized and secreted by the CHIEF CELLS of parathyroid glands
- 48 amino acids
- prephormon (145 amino acids)
-
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
-
second messanger for PTH SECRETON IS BY PARATHYROID GLAND
CAMP
-
SERUM [MG] DECREASED (OR CA)
INCREASE PTH secretion
-
PTH effect
- 1.in kidney and bone DIRECT EFFECT
- 2.small intestine indirect effect through calcitriol
-
PTH function is
- 1.increase Ca reabsorption in thick ascending limb and the distal nephron
- 2.phosphate excretion
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