REGULATION OF K,Ca, PHOSPHATE & MAGNISIUM

• Potassium K regulation

• 4.2+/- 0.3 mEq/L

• Mainly intracellular 2% extracellular

• Excreted mainly by the kidney and 5-10% of the intake by GI

• Factors shift K inside the cell decrease outside:

After meal most of the ingested K moves into the cells until the kid can eliminate the excess.

• A-Insulin

• B-Aldosteron

• C-Beta adrenergic receptors stimulation as increase epinephrine

• D-Alkalosis

• Factors shift K outside the cell

• A-Decrease insulin

• B-Decrease aldosteron

• C-Beta blockers

• D-Acidosis

• E-Cell lysis (muscle injury and RBC lysis)

• F-Sever exercise

• G-Increase extracellular osmolarity

K filtrate, absorbed, secreted and excreted

• 65% of K Reabsorption in the proximal tubule

• And 25-30% reabsorbed in the thick ascending part of loop of Henle as active co- transport along with Na and Cl

•

-Variation in K excretion caused by changes of K secretion in late distal and cortical collecting tubules by principal cell. K in these segments can be absorbed or secreted depend on needs of the body.-During K reduction in the body , intercalated A cells also can reabsorb K(H).Intercalated B cells can also secrete K.

FACTORS REGULATE K SECRETION1- Increase K Concentration in ECF2-Increase aldosteron:Stimulate active

reabsorption of Na through Na-K ATPase3-Increase K in ECF stimulate aldosterone

secretion4-Increase tubular flow rate as with high salt

intake which decrease aldosterone and increase flow rate which counterbalance

each other so little change in K excretion and vice versa

5-H ion concentration(Acidosis) in ECF : acute cause decrease K excretion, chronic cause increase K Loss by: decproximal tubule Na,Cl,H2O absorption and which increase distal vol delivery.Population diet high in K and low in Na do not develop age related hypertension and CV diseases.

CONTROLL OF Ca++ EXCRETIONAND ECF Ca ion CONCENTRATION

• 99% in the bone

• 1% Intracellular

• 0.1% extracellular fluid

• Total Ca in the plasma 5mEq/L:

• 50% ionized form

• 40% Bound with plasma protein

• 10% Complexed with Phosphate &citrate

• Hypocalcemia ^ nerve and muscle excitability and can cause tetany

• Hypercalcemia depress excitability and can cause arrhythmia.

• With acidosis less Ca bound to plasma protein and alkalosis can cause hypocalcemic tetany.

• Main Ca excretion in feces

• PTH is the most important regulator of bone uptake and release of Ca (Endocrine) by:

• 1-Stimulate bone resorption

• 2-Activation of vit D which ^ Ca absorption from GIT

• 3-^ directly renal tubular Ca reabsorption.

•

Control of Ca excretion by the Kid:

• 99% of filtrated Ca is reabsobed same patern as for Na :

• 65% in the proximal tubule:Para & transcellular

• 25-30% in loop of Henle:Thick ascending limb, para & transcellular stimulated by PTH

• 4-9% in the distal & collecting tubules (Active)

Control of Ca absorption1-PTH increase Ca absorption in distal & collecting tubules.2-Ca absorption ^ with ^ plasma phosphate concentration and metabolic acidosis

• Decrease renal Ca excretion with

• 1-^ PTH

• 2-Decrease extracellular fluid

• 3-Decrease BP

• 4-^ Phosphate

• 5-Metabolic alkalosis

• 6-Vit D

RENAL PHOSPHATE REGULATION

• Renal Phosphate regulation :It has transport maximum about 0.1mmol/min.

• Threshold about 0.8mM/L

• 75-80% absorbed in proximal tubule, distal tub 10% and 10% excreted.

• Phosphate concentration about 1mM/L

• ^PTH decrease tubular phosphate absorption & ^ excretion (more with endocrine).

MAGNESIUM

• Control of renal Magnesium :

• 50% in the bone

• Rest within the cell

• Less than 1% in the extracellular fluid.

• Total plasma Mg concentration is 1.8 mEq/L & 50% of this bound to plasma protein, only 0.8mEq/L freely ionized Mg .

• Kidney excrete 10-15% of filtrated Mg

• Mg absorption:

• 1-25% in the proximal tubule

• 2-65% in the loop of Henle

• 3-5% distal & collecting tubules.

• Mg excretion ?? ^ with

• 1-^Mg concentration in ECF

• 2-^ ECF vol

• 3-^ ECF Ca concentration.

INTEGRATION OF RENAL MECHANISM FOR CONTROL OF ECF

• 1-ADH & Thirst mechanisms

• 2-Na absorption and excretion (steady state condition)

• 3-Na Excretion is control by change GF or tubular reabsorption rate

• 4-Pressure natriuresis & Pressure diuresis as in case of increase fluid and salt intake and B.P. regulation

• 5-Sympathetic stimulation

• A-Constriction of renal arterioles and dec GFR

• B-^absorption of salt and water

• C-Increase of Angiotensin II & aldosteron

• 6-Role of Angiotensin II in control renal excretion

• (The most powerful controller of Na excretion)

• 7-Role of aldosterone:Retain Na & H2O & excrt K

• 8-Role of atrial natriuretic peptide: Small changes

Increase Na intake in normal person can cause slight increase in ECF volume and this triggers the followings mechanisms1-Actvate low pressure receptor reflex to inhibit sympactivity2- Suppress angiotensin II formation3-Stimulate natriuretic system ANP.If high Na intake continuo for months or years, kid damage may develop which can lead to hypertension

• Increase Blood volume and Extracellular fluid:

• 1-Congestive heart failure

• 2-Pregnancy increase capacitance of circulation

• 3-Large varicose veins : Increase capacity

• Increase extracellular fluid with normal blood volume:

• 1-Nephrotic syndrome :Proteinuria decrease colloid osmotic pressure and incr cap permeability to fluid and increase absorption of Na and H2O by the kid cause edema

• 2-Liver cirrhosis : Decrease formation of protein and similar events occur as in nephrotic syndrome.