It's not part of the syllabus, but it'd be great to have this as an example in mind for how homeostasis is maintained in relations to balancing water/salt levels in the blood.
In brief: when water levels are too low in the blood, the adrenal cortex in the kidneys releases Aldosterone which stimulates the kidneys to reabsorb the salts in the blood, causing more water to be in the blood (the result of this is that more concentrated urine is released). Conversely, when water levels are too high in the blood, ADH released by the adrenal cortex stimulates the kidneys to reabsorb less sodium, and more water is released by the body as dilute urine instead to restore blood-water balance
Your statements about aldosterone are correct but several statements about ADH require amendment:
1. ADH (also called vasopressin) is produced by the
hypothalamus and released by the
posterior pituitary.
2. The action of ADH on the kidney
increases water reabsorption (by increasing the number of water channels called aquaporins so that water can move back into the blood).
3. ADH is released when the blood is hypertonic (usually when water level is too
low).
4. When water levels are too high, ADH release is
suppressed. With
less ADH released, the aquaporin channel proteins quickly degrade and therefore less water is able to be reabsorbed, resulting in more water excreted as dilute urine.
5. ADH only directly regulates water and doesn’t directly control sodium (although of course the concentration of sodium in the blood is determined by the relative amounts of sodium and water).
6. Sodium is regulated by aldosterone (which you correctly state increases sodium reabsorption) and by
natriuretic peptides (ANP & BNP), which oppose the effects of aldosterone.