I agree with the dehydration diagnosis.  I, too, use the water trick when I
do any serious drinking.  It really works!

Who ?

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It was so much easier to blame it on Them. It was bleakly depressing to
think that They were Us. If it was Them, then nothing was anyone?s fault.
If it was Us, what did that make Me ? After all, I?m one of Us. I must be.
I?ve certainly never thought of myself as one of Them. No-one ever thinks
of themselves as one of Them. We?re always one of Us. It?s Them that do
the bad things.        <=> Terry Pratchett. Jingo.

I suggest the hangover is due to excessive cortisol.

Clin Endocrinol (Oxf). 1995 Jan; 42(1): 65-71.    
The acute effects of oral ethanol on the hypothalamic-pituitary-adrenal axis in
normal human subjects.

Inder WJ, Joyce PR, Wells JE, Evans MJ, Ellis MJ, Mattioli L, Donald RA.

Department of Endocrinology, Christchurch Hospital, New Zealand.

OBJECTIVE: To evaluate the acute effects of oral ethanol on the
hypothalamic-pituitary-adrenal axis in normal human subjects and, in particular,
to examine the effect of background alcohol intake and gastrointestinal
side-effects on this response. DESIGN: Plasma ethanol, cortisol, ACTH,
corticotrophin-releasing hormone (CRH) and AVP were measured half-hourly for 4
hours following 1.1 ml/kg of 95% ethanol or placebo in a cross-over study. At
least one week elapsed between each procedure. SUBJECTS: Twelve healthy
non-alcoholic volunteers with a wide range of background alcohol intakes.
MEASUREMENTS: Peptide hormones were measured by radioimmunoassay, cortisol by
ELISA and blood ethanol by headspace gas chromatography. Results are expressed
as mean +/- SEM. RESULTS: Blood ethanol levels peaked at one hour post ethanol
ingestion. Three subjects developed significant gastrointestinal (GI)
side-effects, with two vomiting and one experiencing moderate to severe nausea.
There was no difference between peak blood ethanol levels in the groups with and
without GI side-effects (34.5 +/- 2.4 mmol/l vs 34.3 +/- 1.7 mmol/l
respectively). ACTH and cortisol rose in those subjects who experienced GI
side-effects (P < 0.0001 for each). The remaining subjects had a tendency for
ACTH and cortisol to be higher on the placebo day. The group with GI
side-effects following ethanol administration had a significant rise in AVP (P <
0.02) that was synchronous with ACTH and cortisol. No consistent alcohol related
changes were seen in peripheral CRH levels, although there was a significant
increase over time on both active and placebo days (P < 0.0001). In the group
with no GI side-effects, AVP did not significantly fall in the first half hour
following ethanol, while a significant fall did occur following placebo (P <
0.05). Plasma renin activity was, however, increased by ethanol (P < 0.05). The
background alcohol intake of the group with GI side-effects was significantly
lower than the group without (18 +/- 7 vs 235 +/- 51 g/week, P < 0.05), but no
hormonal response was seen in two subjects with a relatively low alcohol intake
(< 100 g/week) who did not experience GI side-effects. CONCLUSION: Intoxicating
levels of ethanol per se do not result in activation of the
hypothalamic-pituitary-adrenal axis in humans. However, gastrointestinal
side-effects induced by the ethanol do result in such activation, which appears
to be mediated by AVP as the dominant ACTH secretagogue. One of the factors
which influences the blood ethanol level at which GI side-effects occur appears
to be background alcohol intake.