That's a bit of a complicated question, actually. Let's start with a definition of dehydration. The term is a bit nebulous. In it's simplest use, dehydration is the loss of total body water without loss of sodium, such as you might get with a condition like Diabetes Insipidus. However, I think often the term is used to describe a hypotonic loss of fluid, meaning a greater loss of total body water than total body sodium, this can occur with excessive sweating, infant diarrhea, or osmotic diuresis. Although they are similar states, it's a bit important to distinguish the two the latter state is more severe, leading to signs and symptoms of volume depletion and ultimately to hypovolemic shock (loss of TBNa is always going to give you signs of volume depletion, period).
That said, both are going to result in a high serum sodium (hypernatremia), which is the primary determinant for your plasma osmolality. Thus, you would expect your POsm to go up. Let's take the more likely case here and say it was a really hot day and you were running a marathon without adequate water intake. You are sweating excessively. When you sweat, you lose a hypotonic solution, meaning you lose more water than salt. Both your TBW and your TBNa would go down, but your TBW would go down more, making you appear hypernatremic. Since your TBNa went down, too, you are going to be volume-depleted as well. So, to summarize, you have an increased POsm and you are hypovolemic. Your brain releases ADH in response to the increase in plasma osmolality, causing increase free water reabsorption in your collecting ducts, concentrating your urine. This will normalize your plasma osmolality and prevent further loss of water, but it cannot fully address your hypovolemia (volume depletion). Luckily, you have sensitive baroreceptors which will detect the decrease in fluid volume. Your sympathetic nervous system responds and you are going to have an increase in heart rate, cardiac contractility, vasoconstriction of your peripheral resistance arterioles, and the activation of the Renin-Angiotensin-Aldosterone System (RAAS). If you are hypovolemic enough, your kidney is going to sense the decrease in CO, which further activates your RAAS because of the decreased renal blood flow to your afferent artery. So, renin converts angiotensinogen to AT-1 and ACE in your lung is going to convert AT-I to AT-II. AT-II vasoconstricts your arterioles and, in your zona glomerulosa of your adrenals, stimulates the conversion of corticosterone to aldosterone, by acting on 18-hydroxylase. Aldosterone will act on your Na-K channels in the late distal tubule and collecting duct to absorb reabsorb Na (which brings water along with it). Aldosterone will reabsorb roughly isotonic fluid back into your system. The combined effect of ADH and aldosterone results in reabsorption of roughly hypotonic fluid back into your system to fix your hypotonic fluid loss. AT-II is also going to stimulate thirst and make you want to drink (hopefully with glucose/water solution) and increase water reabsorption in your gut. Therefore, I think the answer to your question is that you would need the actions of both hormones to address your "dehydration."
If you have central DI, you aren't going to become hypovolemic, because you've lost total body water, but you haven't changed your total body sodium. You are going to have a totally normal physical exam and not show any signs of volume depletion. However, you are going to show hypernatremia and an increase POsm in your labs, and as soon as you give desmopressin, boom, you are going to start concentrating your urine and lowering your POsm.
Well, I don't know if I've addressed your question, but this is about all that I know. Perhaps it was not enough in some areas, but too much in others. Oh well.
