ADH vs aldosterone

[Shams al Deen]

Physiology question:

You have someone eat a super salty meal. He is not allowed to urinate. You then measure his serum ADH, renin, and aldosterone.

I know ADH goes up for sure (ADH is very sensitive to serum osmolality), but I'm unsure of renin-angiotensin-aldosterone.

So does RAAS get activated from over-eating some very salty food?

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[Taco Time]

No, I don't think that the RAAS would get activated.

The reason is that when there is increased Na+ intake --> thirst center is activated --> ADH is released --> leads to an increased volume state overall (in the ECF) --> increased BP + heart contracts with a greater force (Frank-S mechanism, due to increased volume state) --> organs shouldn't be under-perfused --> Kidneys shouldn't need to initiate RAAS

The only way I can see it activating RAAS is if the question says that this is an older patient with an extensive history of comorbidities like atherosclerosis where the blood flow is so severely inhibited in such an acute setting, that the kidney initiates RAAS to bring in more blood flow, regardless of the salty meal. The stem could also use a healthy patient who has an acute renal injury that needs to jumpstart the RAAS, but I think it would be fairly obvious from the stem if either of these were to be the case.

But, if the stem of the question essentially had a patient taking in a ton of salt all of a sudden, which is most likely the case, I think it'd be best to assume the former rather than the latter.

 

[Phloston]

Physiology question:

You have someone eat a super salty meal. He is not allowed to urinate. You then measure his serum ADH, renin, and aldosterone.

I know ADH goes up for sure (ADH is very sensitive to serum osmolality), but I'm unsure of renin-angiotensin-aldosterone.

So does RAAS get activated from over-eating some very salty food?

Whether the guy urinates or not won't even make a difference btw. Point being the urine has already gone through the kidney and is either sitting in his bladder or has left his body.

ADH will change with volume, yes, but is more sensitive to changes in tonicity. Therefore the primary response from a salty meal is by ADH. Aldosterone is more affected by changes in volume (e.g., HY --> metabolic alkalosis secondary to aldosterone production secondary to volume contraction due to chronic vomiting, independent of stomach acid loss).

Salty meal would mean a compensatory increase in ADH in order to reduce the tonicity of the blood via free H2O absorption.

Increased free H2O absorption means subtle increase in blood volume, which means renin should decrease in response. If renin is down, then aldosterone is also down.

Another way of thinking about it is aldosterone normally increases sodium reabsorption. If your sodium level is high in the blood, you'd be disinclined to activate that mechanism. (Although in truth, higher sodium levels in the blood are more an activator of ADH versus a suppressor of aldosterone.) In addition, angiotensin-II directly increases sodium reabsorption in the PCT, so you'd be disinclined to activate that response as well (i.e., you'd desire a decrease in renin upstream).

 

[dnnash]

As others have said, the increased sodium concentration will activate ADH and thirst to bring the [Na] back to normal, but will do so by increasing the volume overall. In addition, as long as the ECF osmolarity is high, water will flow from from ICF to ECF to equalize the osmolarity, increasing ECF volume even more. This will downregulate RAAS, which is normally in place to restore GFR/ECF volume when renal perfusion is low.

But don't forget that after you have all this volume, your heart will release ANP and BNP. This will increase GFR to help the body get rid of the sodium and water it has accumulated and bring everything back to normal.

Notice that if you eat a bunch of salt but deny your body water, the only way the osmolarity can get back down is by drawing water from ICF to ECF. You will have a transient increase in ECF volume and ANP and BNP will cause you to lose it. But, what you're left with is normal ECF volume, reduced ICF volume, and slightly increased osmolality (movement of water from ICF>ECF can only bring it partially back down). This is why salt dehydrates you