Effects of clorgyline and (-)deprenyl on the deamination of normetanephrine and noradrenaline in strips and homogenates of the canine saphenous vein.

The influence of specific inhibitors of MAO A (clorgyline) and MAO B [(-)deprenyl] on the metabolism of normetanephrine (NMN) in strips of canine saphenous vein was studied, both in the absence and in the presence of inhibitors of neuronal (cocaine) and extraneuronal (hydrocortisone) uptake. Moreover, the formation of metabolites of noradrenaline and of NMN by saphenous vein homogenates and the influence of clorgyline or (-)deprenyl on this formation are described. Clorgyline reduced to the same degree (by about 70%) the formation of methoxy-hydroxy-phenylglycol (MOPEG) and of vanillylmandelic acid (VMA) in strips incubated with NMN, whereas (-)deprenyl reduced by about 50% the formation of MOPEG and had no effect on VMA production. Hydrocortisone had effects very similar to those of (-)deprenyl. Saphenous vein homogenates (O-methylation inhibited), deaminated both noradrenaline and NMN; clorgyline and (-)deprenyl reduced the formation of metabolites of both noradrenaline and NMN. It is concluded that both MAO A and B are able to deaminate noradrenaline and NMN, but that in the intact tissue the former has no access to MAO B. Even in intact tissues MAO B may play a role in the metabolism (but not in the inactivation) of noradrenaline by deaminating the NMN formed from noradrenaline and giving preferentially origin to MOPEG.