Good question, as ADH (vasopressin), not aldosterone, is actually the main tonicity regulator (via free H2O reabsorption), despite the fact that you'd think this is aldosterone's role because of its stimulation of sodium reabsorption. Yes, ADH will change with volume status, but aldosterone instead is the primary volume regulator, versus vasopressin being tonicity.
There's no set rule for where sodium will fall, but yes, it is the odd one out generally (of Na+, K,+ HCO3-, in aldosterone disorders). Classic pattern for the USMLEs (high aldosterone) is high Na+, low K+, high HCO3- (low H+). I'd say (and this is an arbitrary guess based on my experience), that about 6/10 of QBank and NBME questions will follow this pattern. About 3/10 will have sodium as in the normal range, but slanted toward the direction you'd expect it to go. And about 1/10 will have EVERYTHING NORMAL.
The latter is HY for the USMLE actually. If you're pushed into a position where it's undeniable the aldosterone is high/low and everything is normal, you're not mistaken; aldosterone actually is high/low, and the clinical take-home point is when you're a doc on the wards, you don't just throw away a DDx so hastily because some bloods don't show what you were taught in med school.
But to answer your question, it's possible that with volume augmentation in the setting of high aldosterone, ADH could decrease slightly to compensate, which means lesser free H2O reabsorption and higher serum tonicity. If you ran a serum ADH, it would be normal, but it's not the absolute value that matters; it's how the baseline levels factor into homeostasis among the other bodily systems. Angiotensin-II, btw, is a potent stimulator of PCT Na+ reabsorption (among other things). We know whether we have Conn syndrome (low ATII) or eg a reninoma (high ATII), that doesn't relate to the patient's serum sodium per se (just mentioning that as a counterpoint to an ATII argument).
