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I know that osmolarity is controlled by the hypothalamus and recover by ADH which reabsorb water. It also can be released when ECV is very low.

ECV/salt is controlled by aldosterone/atrial natriuretic peptide which absorbs/releases water and sodium, the ECV is monitored by pressure sensors.

I'm confused about the steady-state. Let's say you drink 2 glasses of water ADH will be blocked in response to reduced osmolarity which makes you urinate more dilute water. But why wouldn't atrial natriuretic be released because drinking water will increase the volume of blood and stretches pressure sensors and then release atrial natriuretic which releases water and sodium to the blood?

My guess is that the pressure sensors can't detect that low of increase in blood pressure because of all the buffering to the intracellular compartment. But how can it detect when we consume salt, it seems like it is still low of increase in blood pressure.

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