gus1 k6_tubular reabsorption and secretion gus-k6
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Early Filtrate Processing
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In the early tubular segment of the
nephron reabsorb solutes and water of the
filtrate back into the blood to restore its
volume and composition. They also
remove some solutes from the blood and
secrete them into the filtrate to fine tune
the bloods composition
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Gambaran seluler dari tubulusrenalis
Tubulus proximal: simple cuboidal cells(brush border cells ok terdapat microvilli)
Thin loop of henle: simple squamous cell,highly permeable to water not to solute
Thick ascending loop of henle & earlydistal tubule: cuboidal cells, highlypermeable to solutes, particularly NaCl butnot to water
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Late distal tubule and cortical collectingduct: cuboidal cells has two distinctfunction:
1. principal cells; permeability to water
and solutes are regulated by hormonesand,
2. intercalated cells; secretion of hydrogen
ion for acid/base balancing
Medullary collecting duct; principal cells;hormonally regulated permeability to
water and urea
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Tubular Reabsorption
By passive diffusion
By primary active transport: Sodium
By secondary active transport: Sugars andAmino Acids
Endositosis ; small proteins and peptide
hormones
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Reabsorption Pathways
There are two reabsorption pathways:
1. the transcellular pathway (>>)
2. the paracellular pathway
To be reabsorbed into the blood, substances
in the filtrate must cross the barrier
formed by the tubular cells.
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Reabsorpsi Filtrat
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Trancellular pathway : Through luminal
and basolateral membranes of the tubularcells into the interstitial space and theninto the peritubular capillaries.
Paracellular pathway : through the tightjunctions into the lateral intercellularspace.
Water and certain ions use bothpathways, especially in the proximalconvoluted tubule.
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Diffusion of WaterWater diffuses from the lumen through the
tight junctions into the interstitial space:
1. Water will move from its higherconcentration in the tubule through thetight junctions to its lower concentration in
the interstitium. 2. Water will also move through the
plasma membranes of the cells that are
permeable to waterAir dapat berdifusi di seluruh bagian
tubulus kecuali di thick segment of theascending limb loop of Henle
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Sodium ReabsorptionDapat mengalami reabsorpsi di seluruh tubulus kecuali
thin segmeny of the limb Loop of Henle
Keluar dari sel ke
interstiital
Lumen
Plasma
Cells
PUMP: Na/K ATPase
Sodium
Potassium
Chloride
Water
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Tubular Secretion
Protons (acid/base balance)
Potassium
Organic ions Zat-zat lain yg tidak normal ada dalam
darah spt obat-obatan dan bahan-bahan
toksik
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Transport Maximum (Tm)
For most actively reabsorbed solutes, theamount reabsorbed in the PCT is limited only bythe number of available transport carriers forthat specific substance.
This limit is called the transport maximum, or Tm.
If the volume of a specific solute in the filtrateexceeds the transport maximum, the excess
solute continues to pass unreabsorbed throughthe tubules and is excreted in the urine.
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Reabsorption: Receptors can Limit
Figure 19-15: Glucose handling by the nephron
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Renal threshold of the plasma- past this
point the kidney cannot reabsorb any
longer and substance will be secreted (ie:
too much glucose). Minimal 225 mg/minglucose Tm pada beberapa nefron
Renal treshold; ambang maks konsentrasi
zat dalam darah yg tidak dijumpai dalamurin
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The final processing of filtrate in thelate distal convoluted tubule andcollecting ducts comes under directphysiological control in response tochanging physiological conditions and
hormone levels. Membrane permeabilities and cellular
activities are altered in response to the
body's need to retain or excrete specificsubstances.
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Distal Tubule & Collecting Duct
The Late Distal Tubule & CCT arecomposed of principal cells & intercalatedcells
Intercalated cells secrete hydrogen ionsinto filtrate
Principals cells perform hormonally
regulated water & sodium reabsorption &potassium secretion
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Role of Aldosteron
Principal cells are more permeable tosodium ions and water in the presence of
Aldosterone & ADH
Low level of Aldosterone result in littlebasolateral sodium/potassium ATPase ionpump activity & few luminal sodium &
potassium channel
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Aldosteron increases the number of
basolateral Na/K pump and luminal Na& K channels
Since there are no basolateral K
channel, K ion are secreted into theinstead of returning to the interstitium
Without an increase in waterpermeability, the interstitial osmolarity
increases
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Role of ADH
Principals cells are more permeable to
water on the presence of ADH
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80% of the blood goes back, only 20% of
the volume is filtered. Of this 20%, only
19% will be reabsorbed.
-total volume that is filtered is only about
180L/day, and 1% of this will excreted.
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Reabsorption in Proximal Tubule
Glucose and Amino Acids
67% of Filtered Sodium
Other Electrolytes 65% of Filtered Water
50% of Filtered Urea
All Filtered Potassium
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Juxtaglomerular apparatus
As the thick ascending loop of henletransition into early distal tubule, the
tubule runs adjacent to the afferent andefferent arteriole.
Where these structure are contact they
form the monitoring structure called thejuxtaglomerular apparatus (JGA), which iscomposed macula densa and JG cells
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Figure 19-9: The juxtaglomerular apparatus
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TUBULOGLOMERULAR FEEDBACK &GLOMERULOTUBULAR BALANCE
Signals from the renal tubule in each nephronfeedback to affect filtration in its glomerulus. As therate of flow through the ascending limb of the loopof Henle and first part of the distal tubule increases,glomerular filtration in the same nephron decreases,and, conversely, a decrease in flow increases theGFR
This process, which is called tubuloglomerularfeedback, tends to maintain the constancy ofthe load delivered to the distal tubule.
The sensor for this response is the macula densa.
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The amount of fluid entering the distaltubule at the end of the thick ascending
limb of the loop of Henle depends on theamount of Na+ and Cl in it.
The Na+ and Cl enter the macula densa
cells via the Na
K
2Cl cotransporter intheir apical membranes.
The increased Na+ causes increased Na, K
ATPase activity and the resultantincreased ATP hydrolysis causes moreadenosine to be formed.
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Presumably, adenosine is secreted from thebasal membrane of the cells. It acts via
adenosine A1 receptors on the macula densacells to increase their release of Ca2+ to thevascular smooth muscle in the afferent
arterioles. This causes afferent vasoconstriction and a
resultant decrease in GFR.
Presumably, a similar mechanism generates asignal that decreases renin secretion by theadjacent juxtaglomerular cells in the afferent
arteriole but this remains unsettled
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Conversely, an increase in GFR causes anincrease in the reabsorption of solutes,and consequently of water, primarily inthe proximal tubule, so that in general thepercentage of the solute reabsorbed is
held constant.
This process is called glomerulotubularbalance, and it is particularly
prominent for Na+.
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The change in Na+ reabsorption occurs withinseconds after a change in filtration, so it seemsunlikely that an extrarenal humoral factor isinvolved.
One factor is the oncotic pressure in theperitubular capillaries.
When the GFR is high, there is a relatively largeincrease in the oncotic pressure of the plasmaleaving the glomeruli via the efferent arterioles andhence in their capillary branches.
This increases the reabsorption of Na+ from thetubule. However, other as yet unidentifiedintrarenal mechanisms are also involved.
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Sympathetic control
In extreme stress or blood loss,sympathetic stimulation overrides the
autoregulation
Increased sympathetic discharge causeintense constriction of renal blood vessel
Blood is shunted to other vital organs GFR reduction causes minimal fluid loss
from blood
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Reduction filtration can not go indefinitely,a waste product build up & metabolicimbalances increase in blood
IV fluid increases blood volume restoresblood pressure to resting levels reduced
sympathetic stimulation allows for normal
arteriole diameter GFR & filtrate flow isnormalized
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Sympathetic Regulation of GFR
Insert fig. 17.11
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