هللامسب Na regulation: Na concentration in the extracellular compartment is 140 meq\l. Na is important because: -It determines the volume of extracellular fluid : the more Na intake will expand extracellular fluid. -It is related to blood pressure. -Na reabsorption in kidney is coupled with reabsorption of glucose, amino acids, phosphate in the proximal tubule by active transport. -Na reabsorption in the thick ascending limb of Henle, increases its concentration in the interstitium so help the kidney in concentrating urine and conserve water. -Na counter transported with H+, so plays a role in acid-base balance. -It also exchange with K. Aldosterone reabsorbs Na and secretes K. The average Na intake is 155mEq\day. 150 meq is removed by kidney and 5 meq by other routes. We take Na more than we need ( the ideal intake is 4 g). We excrete 150 meq in urine so urine concentration is 150/1.5= 100 ( 1.5 urine output) Clearance =100/140=.8
Filtered load= GFR * plasma concentration = 180L\day * 140mEq\L=25200mEq\day (filterad load means how much Na enter bowman's capsule per day?) 99% of filtered load Na is reabsorbed : 65% reabsorbed at the proximal tubule along with water ( in the 1 st half of tubule Na reabsorbed with a.a, glucose. In the 2 nd half is reabsorbed with cl) 25% reabsorbed at the ascending limb of Henle.( Na,k,2cl cotransport) 0 at the descending limb 5% at the distal tubule 4% collecting duct.7% excreted in urine Diuretics work by inhibiting Na reabsorption, it remains in the tubule and drag water with it so secrete more Na and water. They are classified into 3 groups according to their strength which depend on the segment they work in: -strong diuretics work on early loop of Henle and are K wasting.ex: lasix ( furosemide). -intermediate diuretics work at the late loop of Henle and are K wasting. Ex. Thiazide. After two weaks they work as vasodilator -weak diuretics work at the distal tubule and are K sparing. Ex. Aldactone which is aldosterone antagonist.
If Na intake is reduced or increased the kidney can handle it with no hypo- or hypernatremia. In contrast to K ( if the intake is low you will suffer hypokalemia. The mechanism for Na control: If the intake is increased, the volume will be expanded stretching the atrium so ANP( Atrial Natriuretic Peptide) will be secreted ( also called ANH). ANP functions: 1)decrease Na reabsorption from distal part. 2)decrease aldosterone secretion from adrenal cortex. 3)dilate afferent arteriole:increase blood flow to glomerulus and thus increasing GFR. and it is the only hormone which increase Na secretion. SO in conclusion we control Na homeostasis by: altering GFR or reabsorption capacitances. Kidney function curve:.
If we increase Na intake twice, blood pressure will increase unless thecurve is shifted to left. Shifting the curve is by decreasing production of angiotensinogen II ( decrease Na reabsorption). Renal failure patients shift the curve to right(they already have hypertension so we must ask them to reduce Na intake to bring blood pressure to normal). K regulation: K intake is 100 meq Excretion is also 100 meq( 95 is removed by kidney, 5 by other routes so kidney is a major regulator of K). K is very important because the cell membrane is most permeable to it, so resting membrane potential(rmp) is very close to the equilibrium potential of K. according to Nernest equation Ek= -61 log( k inside/k outside) = -61log( 150/4)=-90 mv If I increase the extracellular K, what will happen? 1)The more the K concentration the less the negativity of RMP, so there is more excitability. 2)fast Na channels are not able to open so conduction will be through slow Na channel and this turn the cell from fast response to slow.
Less k makes cell less excitable. Both situations are dangerous. A patient with renal failre will have hyperkalemia ( K concentration will reach 7mEq ) should be admitted immediately for hemodialysis, if not available we use peritoneal dialysis. Filterd load of K= 180L/day * 4mEq/L = 720mEq/ day Reabsorption of K: 80% at the proximal tubule ( it is very active so rich in mitochondria) 10% at the ascending loop of Henle 10% will be excreted = 72 but 100 meq should be excreted as we said previously, so 30 meq wil be secreted actively. K is controlled by filteration,reabsorption,secretion. But Na by filtration and reabsorption only. If you take 200 meq/dayof K, you will secrete 128 and filter 72, so secretion plays a major role in controlling K.
If you eat meal rich in K you will take for example, 50 mmole,and when they get distributed in the extracellular space (14 L) THE k will reach 7.5 (50/14 + 4). 4( normal K level). How the body controlsthis situation? 1)insulin hormone which push K inside cells( if a patient come with hyper kalemia give him insulin with glucose to avoid hypoglycemia). 2)aldosterone which is secreted from zona glomerulosa and works on the distal tubule. It inserts Na channels at the apical side of the tubular cell ( Na enters the cell, stimulate na, k pump, increase k gradient so increase its secretion). If adrenal gland makes too much aldosterone this is called conns disease.it causes hypertension and hypokalemia. We must measure k levels for a hypertensive patient, if its high we exclude conns. Some diuretics cause hypokalemia. 3) acid base status should be regulated ( if a patient has acidosis the body try to push H inside the cell and K go out to maintain electrical balance, so he will complain hyperkalemia). Calcium regulation: 99% of ca reside in bones.
The normal concentration of Ca+2 extracellularly is about 1mmol/L. The normal concentration of Ca+2 intracellulary is about 10^- 7-10^-9mol/L. The ca concentration was measured by micropipettes. Calcium is regulated by 3hormones, and 3 organs. Hormones that regulate calcium are: a) Calcitonin. b) Parathyroid hormone.c) Vitamin D. Organs that regulate calcium:a) Bones.b) GI Tract.c) Kidneys. Parathyroid decrease Ca reabsorption in proximal tubule but increase it in the distal tubule. IN GENERAL increase CA reabsorption. reabsorption of Calcium 65% in the proximal tubules. 25% in the ascending limb of Henle. 8 % in distal tubules. 1% in the collecting duct. 1% excreted. Most kidney stones are calcium oxalate. Hypercalciruea is treated by: 1)Giving thiazide which increase ca reabsorption.but lasix increase ca excretion.
2)ask the patient to drink a lot of water so ca is diluted. 3)reduce salt intake. Done by: Raghad Mujalli