EFFECT OF SOME NEWER MONOAMINE OXIDASE INHIBITORS ON CATECHOLAMINE INDUCED PRESSOR RESPONSES

Role of monoamine oxidase in the metabolism of epinephrine and norepinephrine has not so far been fully established. In man and rodents Axelrod (1) has postulated that o-methylation is the first and principal step in the metabolism of catecholamines and that the methylated derivatives of epinephrine (metanephrine) and norepinephrine (normetanephrine) undergo further oxidative deamination by monoamine oxidase. Such an inactivation of catecholamines has been reported by Axelrod (1) and Whitby et al. (2) to be dependent upon tissue and species variations. Furthermore, differences observed between circulating or injected and endogenously released amines have indicated that monoamine oxidase plays an important role in tissue metabolism of catecholamines (3, 4). In the present study attempts have been made to show correlationship between monoamine oxidase inhibition and changes in the vascular effect of injected epinephrine and norepinephrine. Some newer quinazolone hydrazides (5) and quinazolone hydrazines (6) synthesized as monoamine oxidase inhibitors, reported earlier for their anti-convulsant properties (7), were used to investigate their effects on epinephrine and norepinephrine induced pressor responses in cats.