Conversion of MHPG to Vanillylmandelic Acid

Human class I alcohol dehydrogenases catalyze the oxidation of glycols in the metabolism of norepinephrine.

“…The present results are consistent with the facts that VMA (13) is formed as a result of HMPG oxidation in man (14,20,21), that this process is inhibited by ethanol in vivo (14), and that the liver is the major and dominant site of such oxidation (unpublished work (1985) class III (X) ADH (unpublished work); as would then be expected, the amount of VMA in brain is minute (22).…”

Coexisting dysregulations of both the sympathoadrenal system and hypothalamic-pituitary-adrenal-axis in melancholia

“…As a result, since the above-mentioned authors did not adjust their MHPG data for these sources of bias, their results are not interpretable. MHPG levels reflect total body (central + peripheral) catecholamine metabolism (Filser, 1986;Maas and Leckmann, 1983;Blombery et al, 1980), whereas the principal, if not the only source of circulating catecholamines consists of a release from sympathetic nerve endings and adrenal medulla (Essler et al, 1982;Kopin et al, 1984;Lake et al, 1984;Maas et al, 1987). As a result, our data could prove that severe depression is linked to peripheral (i.e.…”

Urinary-free cortisol in depressed patients and controls: relationship to urinary indices of noradrenergic function

“…Most NE released from nerve endings is recaptured and intraneuronally deaminated by monoamine oxidase to dihydroxyphenylglycol; this then diffuses out of the neuron and is O-methylated by catechol-Omethyltransferase (COMT) to MHPG. MHPG is taken to the liver and other organs where it is either oxidized to VMA, or conjugated and excreted in the urine (Blombery et al 1980). However, some released NE from sympathetic nerve terminals escapes reuptake and is Omethylated by COMT, forming NM which is partially conjugated and excreted, or deaminated and excreted as VMA.…”