Influence of harmaline on the ability of pargyline to alter catecholamine metabolism in rats

When pargyline hydrochloride (20 mg/kg, i.p.) was injected into rats 48 hr before the measurement of monoamine oxidase (MAO) activity, the oxidation of [¹⁴C]phenylethylamine (type B MAO) and of [¹⁴C]-serotonin (type A MAO) was inhibited. Neither type A nor type B MAO was inhibited 48 hr after the injection of harmaline hydrochloride (30mg/kg, i.p.) a short-acting, reversible, highly selective inhibitor of type A MAO. When harmaline was given just before pargyline, it prevented the inhibition of type A MAO by pargyline but not the inhibition of type B MAO. Pargyline alone elevated epinephrine, norepinephrine, and dopamine concentrations in brain regions and norepinephrine concentration in heart. The concentration of dopamine metabolites (3,4-dihydroxyphenylacetic acid and homovanillic acid) was decreased. Pretreatment with harmaline prevented all of these effects of pargyline. The findings suggest that inhibition of type A MAO is involved in the inhibition of catecholamine metabolism by pargyline, since harmaline pretreatment did not prevent inhibition of type B MAO and would not be expected to alter any other possible actions of pargyline. These findings support the idea that type A MAO is primarily responsible for the oxidation of epinephrine, norepinephrine, and dopamine in rat brain and of norepinephrine in rat heart.