Control of Na+ excretion.

Dr.Mohamad Shaikhani.Dr.Mohamad Shaikhani.

Control of Na+ excretion. Through:Through:1.ADH.1.ADH.2.Thirst.2.Thirst.3.Salt appetite3.Salt appetite4.Cardiovascular reflexes (BP & blood volume).4.Cardiovascular reflexes (BP & blood volume).

Control of EC Na+& osmolarity:Control of EC Na+& osmolarity:

1.Osmoreceptor ADH feedback system:1.Osmoreceptor ADH feedback system:Na+ is responsible for > 90% of serum Na+ is responsible for > 90% of serum

osmolarity (SO) so if there is increase in SO osmolarity (SO) so if there is increase in SO (S.Na+) this will stimulate the ADH (S.Na+) this will stimulate the ADH osmoreceptor of hypothalamus( located at the osmoreceptor of hypothalamus( located at the supraoptical area & the anteroventral part of supraoptical area & the anteroventral part of the 3the 3rdrd ventricle at which there is no blood ventricle at which there is no blood brain barrier so the Na+& other solutes can brain barrier so the Na+& other solutes can get easily access to this center & stimulate it) get easily access to this center & stimulate it) to secrete ADH into the blood which leads to to secrete ADH into the blood which leads to water reabsorption by the DT & CD & formation water reabsorption by the DT & CD & formation of concentrated urine with high Na+ content & of concentrated urine with high Na+ content & vice versa will occur if there is low SO & low vice versa will occur if there is low SO & low Na+.Na+.

Control of EC Na+& osmolarity:Control of EC Na+& osmolarity:2.Thirst2.Thirst The same osmoreceptor is responsible for The same osmoreceptor is responsible for

stimulating thirst sensation, when there is high stimulating thirst sensation, when there is high SO & S.Na+ the receptor cells will become SO & S.Na+ the receptor cells will become dehydrated &this will stimulate thirst sensation dehydrated &this will stimulate thirst sensation to force the person to drink & correct the water to force the person to drink & correct the water deficit & high SO. deficit & high SO.

After water intake diuresis occurs after 45 mins After water intake diuresis occurs after 45 mins as this time is needed for absorption of water & as this time is needed for absorption of water & destruction of already present ADH,while thirst destruction of already present ADH,while thirst sense is relieved immediately by water intake as sense is relieved immediately by water intake as water distends the esophagus & stomach before water distends the esophagus & stomach before absorption to avoid over dilution of blood. absorption to avoid over dilution of blood.

The ADH & thirst mechanism is effective in The ADH & thirst mechanism is effective in control of S.Na+ at various Na+ intakes.control of S.Na+ at various Na+ intakes.

Control of EC Na+& osmolarity:Control of EC Na+& osmolarity:3.Salt appetite: 3.Salt appetite: The same center for ADH &thirst serves for salt The same center for ADH &thirst serves for salt

appetite ,stimulated by decrease S,Na+& low BP & appetite ,stimulated by decrease S,Na+& low BP & low blood volume, but this is more slow& needs low blood volume, but this is more slow& needs several hours to cause salt craving. several hours to cause salt craving.

Animals search for salt& lick salt called salt licks. Animals search for salt& lick salt called salt licks. Salt craving is most obvious in Addison disease when Salt craving is most obvious in Addison disease when

there is destruction of adrenal cortex with loss of there is destruction of adrenal cortex with loss of aldosterone & decrease serum Na+ & BP.aldosterone & decrease serum Na+ & BP.

4.Cardiovascular reflexes (BP & blood volume): 4.Cardiovascular reflexes (BP & blood volume): Through stimulation of ADH directly or indirectly.Through stimulation of ADH directly or indirectly.

Control of EC Na+& osmolarity:Control of EC Na+& osmolarity:Syndrome of inappropriate ADH secretion:Syndrome of inappropriate ADH secretion: There are several pathological conditions causing There are several pathological conditions causing

excessive ADH secretion, the most common in small excessive ADH secretion, the most common in small cell carcinoma of the lung, this excess ADH causes cell carcinoma of the lung, this excess ADH causes water intoxication by increasing water reabsorption water intoxication by increasing water reabsorption by the DT segments causing water intoxication& low by the DT segments causing water intoxication& low S.Na+ leading to various neuromuscular symptoms& S.Na+ leading to various neuromuscular symptoms& signs.signs.

    

Control of Na+ excretion by Aldosterone Control of Na+ excretion by Aldosterone (ALS).(ALS).

Na+ excretion in (DT) is ALS dependantNa+ excretion in (DT) is ALS dependant While in (PT) is not ALS dependant.While in (PT) is not ALS dependant. 65% of Na+ is absorbed in PT with H20 & it is not 65% of Na+ is absorbed in PT with H20 & it is not

ALS dependant ALS dependant 27% of it is actively absorbed in TALH without 27% of it is actively absorbed in TALH without

water & also not ALS dependant.water & also not ALS dependant. The remaining 8% is absorbed from DTs (late The remaining 8% is absorbed from DTs (late

DT ,cortical CD & medullary CD) & is ALS DT ,cortical CD & medullary CD) & is ALS dependant. dependant.

Urinary excretion of Na+ /day is 0.1 gm In the Urinary excretion of Na+ /day is 0.1 gm In the presence of ALS & 2O gms in its absence .presence of ALS & 2O gms in its absence .

The control of ALS secretion is under:

1. Angiotensin 2 in the blood by activation 1. Angiotensin 2 in the blood by activation of Juxta glomerular apparatus causing of Juxta glomerular apparatus causing activation of Renin angiotensin ALS axis.activation of Renin angiotensin ALS axis.

2.Decrease of EC Na+ & increase in EC K+.2.Decrease of EC Na+ & increase in EC K+. Serum Na+ is well controlled with or Serum Na+ is well controlled with or

without ALS feedback (FB)control without ALS feedback (FB)control because:because:

1. ADH & thirst overiding the ALS FB ,if 1. ADH & thirst overiding the ALS FB ,if ALS is absent.ALS is absent.

2. In hyperaldosteronism, hypernatremia, 2. In hyperaldosteronism, hypernatremia, hypertension& increased GFR occur, hypertension& increased GFR occur, causing increased Na+ excretion,so causing increased Na+ excretion,so returning serum Na to normal (PRESSURE returning serum Na to normal (PRESSURE DIURESIS).DIURESIS).

K+ excretion: Is ALS & serum Na+ dependant in DTS ,But not in PTS & Is ALS & serum Na+ dependant in DTS ,But not in PTS &

TALH TALH .. 65% 65% of K+ is reabsorbed cotransport with Na+ in PT & not of K+ is reabsorbed cotransport with Na+ in PT & not

ALS dependantALS dependant while 27% of it is reabsorbed cotransport with Na+ in the while 27% of it is reabsorbed cotransport with Na+ in the

TALH TALH 4% is secreted into late distal segments under normal 4% is secreted into late distal segments under normal

conditions ,So that normally 12% is excreted to the urineconditions ,So that normally 12% is excreted to the urineK either mainly reabsorbed or mainly excreted according to:K either mainly reabsorbed or mainly excreted according to: The effect of serum K+ or serum ALS ,in the late DT & The effect of serum K+ or serum ALS ,in the late DT &

cortical CD by special cells called Principal cells(PCs) cortical CD by special cells called Principal cells(PCs) through a FB control loop .through a FB control loop .

K+ excretion: The most important factors that stimulate K+ The most important factors that stimulate K+

secretion by PCs are:secretion by PCs are: Increased ECF K+(either directly or through Increased ECF K+(either directly or through

increasing ALS),increasing ALS), High serum ALS( ALS blockade greatly impair High serum ALS( ALS blockade greatly impair

control of K+ concentration).control of K+ concentration). Under conditions of severe K+ depletion it is Under conditions of severe K+ depletion it is

reabsorbed from late DT & CD by intercalated reabsorbed from late DT & CD by intercalated cells.cells.

8%remaining

Regulation of ECV & blood volume: 1 .BV is well controlled in the normal range of 5 Ls. through a feedback loop system as when BV increases it causes increase in cardiac output ,BP & this will cause through 1 .BV is well controlled in the normal range of 5 Ls. through a feedback loop system as when BV increases it causes increase in cardiac output ,BP & this will cause through

pressure natriuresis increase in urinary Na+ excretion so returning the BV towards normal( BV,CO,BP,urine output ,BV feedback loop)& vice versa is true.this is pressure natriuresis increase in urinary Na+ excretion so returning the BV towards normal( BV,CO,BP,urine output ,BV feedback loop)& vice versa is true.this is responsible for control of 90 to 95% of ECF & BV specially in chronic states.responsible for control of 90 to 95% of ECF & BV specially in chronic states.

2.Arterial baroreceptors.2.Arterial baroreceptors. 3 Arterial natriuretic peptides(ANP) when the atria are distended by increased BV.3 Arterial natriuretic peptides(ANP) when the atria are distended by increased BV. 4.ALS. 5.Angiotensin 2. 6.ADH.4.ALS. 5.Angiotensin 2. 6.ADH. The last 5 are responsible for control of 5 to 10% of BV specially in acute states.The last 5 are responsible for control of 5 to 10% of BV specially in acute states.

Causes of increased BVCauses of increased BV 1. Heart failure: as reduced CO causes activation of RA ALS axis 1. Heart failure: as reduced CO causes activation of RA ALS axis

leading to Na+ & H20 retention causing increased BVleading to Na+ & H20 retention causing increased BV 2.Liver cirrhosis: as decreased albumin which is synthesized by 2.Liver cirrhosis: as decreased albumin which is synthesized by

the liver causes decrease BV stimulating RA ALS axis as above.the liver causes decrease BV stimulating RA ALS axis as above. 3 Nephrotic syndrome : as it causes loss of albumin in urine & so 3 Nephrotic syndrome : as it causes loss of albumin in urine & so

decrease BV stimulating RA ALS axis as above.decrease BV stimulating RA ALS axis as above. 4.Polycythemia: as increased RBC mass causes increase blood 4.Polycythemia: as increased RBC mass causes increase blood

viscosity so decrease blood flow, venous return & so CO & BV viscosity so decrease blood flow, venous return & so CO & BV leading to stimulation of RA ALS axis as above.leading to stimulation of RA ALS axis as above.