Regulation of Extra Cellular Fluid Potassium Concentration and Potassium Excretion

7/31/2019 Regulation of Extra Cellular Fluid Potassium Concentration and Potassium Excretion

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Regulation of Potassium BalancePada keadaan normal, konsentrasi potassium dalam

cairan ekstraseluler sebesar 4.2 0.3 mEq/L .

Sebagian besar dari fungsi sel, sensitif terhadap

perubahan konsentrasi potasium ekstraseluler. Apabila

ada kenaikkan konsentrasi plasma potassium, hanya,

sekitar 3 4 mEq/L dapat menyebabkan cardiac

arrhythmias , dan pada konsentrasi yang lebih tinggi

dapat menuju cardiac arrest atau fibrillation .

Kesulitan pada pengaturan konsentrasi potassium

ekstraseluler berdasarkan fakta bahwa lebih dari 98 %

total body potassium berada di dalam sel. Regulasi keseimbangan antara intake dan output potassium bergantung pada ekskresi ginjal karena

ekskresi melalui feses hanya sekitar 5 10 % dari intake potassium.

Selain ekskresi dari ginjal, distribusi potassium antar ekstraseluler dan intraseluler juga berperan dalam

homeostasis potassium. Karena lebih dari 98% total body potasium berada di dalam sel, sel dapat

menjadi tempat menampung potassium ekstraseluler yang berlebih pada hyperkalaemia atau sumber

potassium selama hypokalemia. Jadi, redistribusi potasium menjadi first line of defense dalam

mengatur keseimbangan potassium.

Regulation of Internal Potassium Distribution

Factors That Can Alter Potassium Distribution Between the Intracellular and Extracellular Fluid Factors That Shift K + into Cells(Decrease Extracellular [K +])

Factors That Shift K + Out of Cells(Increase Extracellular [K +])

InsulinAldosterone-adrenergic stimulationAlkalosis

Insulin deficiency (diabetes mellitus)Aldosterone deficiency (Addison's disease)-adrenergic blockadeAcidosisCell lysisStrenuous exerciseIncreased extracellular fluid osmolarity


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Renal Potassium Excretion

Fungsi ekskresi potassium oleh ginjal ditentukan dari ketiga

proses:

(1) kecepatan potassium filtration

(2) kecepatan potassium reabsorption di tubulus

(3) kecepatan potassium secretion di tubulus

Kecepatan filtrasi potassium normal oleh glomerulus sekitar

756 mEq/day. ( GFR (180 L/day) multiplied by plasma

potassium concentration , (4.2 mEq/L))

* Daerah yang penting dalam pengaturan ekskresi potassium

berada pada principal cells di late distal tubules dan

cortical collecting tubules .Pada bagian tubular, potassium dapat sewaktu direabsorbsi atau disekresi, tergantung dari kebutuhan tubuh.

Dengan asupan potassium 100 mEq/day, ginjal harus mengekskresikan sekitar 92 mEq/day (sisa 8 mEq dibuang

melewati feces). Sekitar 31 mEq/day potassium disekresikan ke distal dan collecting tubules , atau sekitar 1 / 3

ekskresi potassium.

Potassium Secretion by Principal Cells of Late Distal and Cortical Collecting Tubules

Sel pada late distal dan cortical collecting tubules yang

mengsekresikan potassium disebut principal cells danterdapat sekitar lebih dari 90% di sel epithelial di daerah

tersebut.

Sekresi potassium dari interstitial ke lumen merupakan proses

dengan dua tahap:

1. uptake from the interstitium into the cell by the

sodium-potassium ATPase pump in the basolateral

cell membrane

2. passive diffusion of potassium from the interior of the cell into the tubular fluid

Membran luminal pada principal cells sangat permeable terhadap potassium. Salah satu alasan tingginya

permeabilitas karena adanya channel yang spesifik untuk ion potassium, memudahkan difusi ion tersebut

dengan cepat.

Intercalated Cells Can Reabsorb Potassium during Potassium Depletion

Pada keadaan dimana terjadi kekurangan potassium yang parah, terjadi penghentian sekresi potassium dan erjadi

reabsorbsi pada late distal dan collecting tubules. Reabsorpsi terjadi melalui intercalated cells. Mekanisme

masih belum jelas, namun satu mekanisme yang dipercaya terlibat merupakan transport dari hydrogen-


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potassium ATPase yang terdapat di membrane luminal. Transporter tersebut mereabsorpsi potassium dengan

menukar ion hydrogen keluar ke lumen dan potasium berdifusi melalui basolateral membrane menuju ke

plasma.

Summary of Tubular Potassium Transport

Transport Normal-or high-potassium dietLow-potassium diet or potassium

depletion

Proximal tubule Reabsorption (60 80%) Reabsorption (55%)

Thick ascending limb Reabsorption (5 25%) Reabsorption (30%)

Distal convoluted tubule Secretion Reabsorption

Principal cells, cortical collecting duct Substantial secretion (> 15%) Little secretion

H-K-ATPase-containing intercalated cells,

cortical collecting ductReabsorption (10%) Reabsorption (10%)

H-K-ATPase-containing cells, medullary

collecting ductReabsorption (5%) Reabsorption (5%)

Factors That Regulate Potassium Secretion

Regulasi normal eksresi potassium terajadi sebagai akibat sekresi potassium pada principal cells di late distal

dan collecting tubules . Faktor yang paling penting pada stimulasi sekresi potassium adalah:

(1) Peningkatan konsentrasi potassium ekstraselular

(2) Peningkatan aldosterone

(3)

Peningkatan tubular flow rate Satu faktor yang menurunkan sekresi potassium adalah peningkatan konsentrasi ion hydrogen (acidosis).

1. Increased Extracellular Fluid Potassium Concentration Stimulates Potassium SecretionKecepatan sekresi di late distal dan cortical collecting tubules distimulasi secara langsung oleh konsentrasi

potassium ekstraseluler. Peningkatan konsentrasi potassium di ekstraseluler meningkatkan sekresi potassium

melalui tiga mekanisme:

(1) stimulates the sodium-potassium ATPase pump

(2) increases the potassium gradient from the renal interstitial fluid to the interior of the epithelial cell.

(3) stimulates aldosterone secretion by the adrenal cortex

2. Aldosterone Stimulates Potassium SecretionAldosterone merangsang active reabsorption dari ion sodium oleh principal cells di late distal tubules dan

collecting ducts. Efek ini dimediasi oleh sodium-potassium ATPase pump. Efek lain dari aldosterone adalah

meningkatkan permeabilitas membrane luminal terhadap potassium, karena itu aldosterone memiliki efek yang

kuat pada peningkatan eksresi potassium.


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3. Increased Distal Tubular Flow Rate Stimulates Potassium SecretionKenaikkan pada kecepatan distal tubular flow, seperti pada high sodium intake, atau pengobatan dengan

diuretics, dapat merangsang sekresi potassium. Mekanisme dari high-volume flow rate: Saat potassium

disekresikan ke lumen tubular, konsentrasi potassium lumen akan meningkat, sehingga menurunkan difusi

potasium melalui membrane luminal. Dengan peningkatan kecepatan tubular flow, potassium yang keluar

dibuang melalui tubule, sehingga konsentrasi potassium di lumen akan sangat minim.

4. Acute Acidosis Decreases Potassium Secretion

Kenaikan konsentrasi ion hydrogen yang akut di ekstraseluler (acidosis) menurunkan sekresi potassium, begitu

juga pada keadaan yang sebaliknya (alkalosis), menaikkan sekresi potassium. Mekanisme utama kejadian

tersebut dsebabkan ion hydrogen yang menghambat sekresi potassium dengan menurunkan akifitas sodium-

potassium ATPase pump.

Dengan adanya acidosis yang lama, terjadi peningkatan eksresi potassium. Mekanisme ini terjadi akibat keadaan

kronik acidosis yang menghambat proximal tubular sodium chloride dan water reabsorption , yang

meningkatkan distal volume delivery, sehingga menstimulasi sekresi potassium. Efek ini melampaui efek

inhibitori dari ion hydrogen terhadap sodium-potassium ATPase pump. Thus, chronic acidosis leads to a loss of

potassium , whereas acute acidosis leads to decreased potassium excretion

Hiperkalemia dapat berhubungan dengan bermacam-macam perubahan pada EKG. Pada keadaan awa l: tall peaked T waves with a shortened QT interval Pada keadaan yang makin parah : progressive lengthening of the PR interval and QRS duration, the P

wave may disappear, and ultimately the QRS widens further to a sine wave pattern.

Pada tahap akhir : Ventricular standstill with a flat line on the ECG ensues with complete absence of

electrical activity


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Potassium Regulation

Potassium is freely filterable in the renal corpuscle. Normally, the tubules reabsorb most of this

filtered potassium so that very little of the filtered potassium appears in the urine. However, the

cortical collecting ducts can secrete potassium, and changes in potassium excretion are due mainly tochanges in potassium secretion by this tubular segment (Figure 16 24).

During potassium depletion, when the homeostatic response is to minimize potassium loss, there is no

potassium secretion by the cortical collecting ducts, and only the small amount of filtered potassium

that escapes tubular reabsorption is excreted. In all other situations, to the small amount of potassium

not reabsorbed is added a variable amount of potassium secreted by the cortical collecting ducts, an

amount necessary to maintain total-body potassium balance.

The mechanism of potassium secretion by the cortical collecting ducts was illustrated in Figure 16

12.

In this tubular segment, the K_ pumped into the cell across the basolateral membrane by Na,K-

ATPases diffuses into the tubular lumen through K_ channels in the luminal membrane.

Thus, the secretion of potassium by the cortical collecting duct is associated with the reabsorption of

sodium by this tubular segment. (Potassium secretion does not occur in other sodium reabsorbing

tubular segments because there are few potassium channels in the luminal membranes of their cells;

rather, in these segments the potassium pumped into the cell by Na,K-ATPases simply diffuses back

across the basolateral membrane through potassium channels located there.)

What factors influence potassium secretion by the cortical collecting ducts to achieve homeostasis of

bodily potassium? The single most important factor is as follows: When a high-potassium diet is

ingested, plasma potassium concentration increases, though very slightly, and this drives enhanced

basolateral uptake via the Na,K-ATPase pumps and hence an enhanced potassium secretion.

Conversely, a low potassium diet or a negative potassium balance, for example, from diarrhea, lowers

basolateral potassium uptake; this reduces potassium secretion and excretion, thereby helping to

reestablish potassium balance. A second important factor linking potassium secretion to potassium

balance is the hormone aldosterone. Besides stimulating tubular sodium reabsorption by the cortical

collecting ducts, aldosterone simultaneously enhances tubular potassium secretion by this tubular

segment.

The reflex by which an excess or deficit of potassium controls aldosterone production (Figure 16 25)

is completely different from the reflex described earlier involving the renin-angiotensin system. The


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aldosterone-secreting cells of the adrenal cortex are sensitive to the potassium concentration of the

extracellular fluid bathing them. Thus, an increased intake of potassium leads to an increased

extracellular potassium concentration, which in turn directly stimulates aldosterone production by the

adrenal cortex.

The resulting increased plasma aldosterone concentration increases potassium secretion and thereby

eliminates the excess potassium from the body.

Conversely, a lowered extracellular potassium concentration decreases aldosterone production and

thereby reduces potassium secretion. Less potassium than usual is excreted in the urine, thus helping

to restore the normal extracellular concentration.

The control and major renal tubular effects of aldosterone are summarized in Figure 16 26. The fact

that a single hormone regulates both sodium and potassium excretion raises the question of potential

conflicts between homeostasis of the two ions. For example, if a person were sodium-deficient and

therefore secreting large amounts of aldosterone, the potassium secreting effects of this hormone

would tend to cause some potassium loss even though potassium balance was normal to start with.

Usually, such conflicts cause only minor imbalances because there are a variety of other counteracting

controls of sodium and potassium excretion.

(1) A person remains in potassium balance by excreting an amount of potassium in the urine

equal to the amount ingested minus the amounts lost in the feces and sweat.

(2) Potassium is freely filterable at the renal corpuscle and undergoes both reabsorption and

secretion, the latter occurring in the cortical collecting ducts and being the major

controlled variable determining potassium excretion.

(3) When body potassium is increased, extracellular potassium concentration increases. This

increase acts directly on the cortical collecting ducts to increase potassium secretion and

also stimulates aldosterone secretion, the increased plasma aldosterone then also

stimulating potassium secretion.


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Regulation of Extra Cellular Fluid Potassium Concentration and Potassium Excretion

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