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Can anyone explain why AT II can lead to contraction alkalosis? (FA pg. 440)

As I know, increase in AT II will ultimately lead to fluid retention, as well as alkalosis. But why the "contraction"?

Do they mean that the "contraction" is by the fluid loss which lead to the increase in AT II, but not directly by the AT II?
 

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Angiotensin II is responsible for the alkalosis part of the contraction alkalosis term, it's not responsible for the contraction. Rather it's the result of contraction.

So what happens, is that when you have decreased ECF, renin and ultimately ATII will increase to compensate for the fluid loss by reabsorbing Sodium.
In the proximal convoluted tubules, Sodium reabsorption is coupled to Hydrogen ion secretion (Na/H Antiport). These secreted Hydrogen ions will dissolve into carbonic acid which in turn dissolve into CO2 and Water. This CO2 and water will be reabsorbed via the action of carbonic anhydrase back into the tubular cell forming bicarbonate which goes into the blood stream causing the alkalosis.

So ATII by stimulating the Na/H antiport will also promote bicarbonate reabsorption and so it's responsible for contraction alkalosis (that's the alkalosis seen in contraction). It's called saline responsive alkalosis.

While in primary hyperaldosteronism the alkalosis is not responsive to saline because it's not the contraction that has caused the alkalosis but the rather the increased aldosterone itself.
 

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What resheed is talking about is nicely illustrated in Kaplan Lecture Notes in the carbonic anhydrase section of the diuretics chapter of the pharmacology book
 

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In addition to the great answers by the members
I like to take the subject of contraction further

Contraction alkalosis result when we use any diuretic except Carbonic anhydrase and aldosterone antagonists (K sparing) diuretics.
There are two reasons for this:
1- by the time urine reaches the collecting ducts (much Na has been prevented from re-absorption by the action of the diuretics proximal) so the collecting duct cell will desperately to reabsorb this overload of Na (but it fails) and in doing so it will also excrete Hydrogen ions to maint electrical neutrality and thereby causing loss of acid and so alkalosis
2- normally bicarb has a low concentration in the urine, so when you have tremendously increased (urine fluid volume by the diuretic) then the concentration of the bicarb in the ECF wich means alkalosis
 

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contraction alkalosis

Contraction alkalosis means :

1.Loss of bicarbonate-poor, chloride-rich extracellular fluid, as observed with thiazide diuretic or loop diuretic therapy or chloride diarrhea or NG tube suction,or vomiting,which leads to contraction of extracellular fluid volume.

2. Because the original bicarbonate mass is now dissolved in a smaller volume of fluid,"contraction" of ECF , an increase in bicarbonate concentration occurs. This increase in bicarbonate causes, at most, a 2- to 4-mEq/L rise in bicarbonate concentration.

The treatment is : adm of 0.9% NaCl.

Hopefully this will clarify further the question.
 

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Contraction alkalosis means :

1.Loss of bicarbonate-poor, chloride-rich extracellular fluid, as observed with thiazide diuretic or loop diuretic therapy or chloride diarrhea or NG tube suction,or vomiting,which leads to contraction of extracellular fluid volume.

2. Because the original bicarbonate mass is now dissolved in a smaller volume of fluid,"contraction" of ECF , an increase in bicarbonate concentration occurs. This increase in bicarbonate causes, at most, a 2- to 4-mEq/L rise in bicarbonate concentration.

The treatment is : adm of 0.9% NaCl.

Hopefully this will clarify further the question.
Thank you for the great explanation
 
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