STIMULATORY EFFECT OF RESERPINE ON MONOAMINE OXIDASE IN GUINEA PIG HEART

(1) In slices, homogenates or mitochondrial fractions of the hearts of guinea pigs after reserpine treatment, the amounts of deaminated metabolites of 14C-norepinephrine were more than in the controls. This seems to be because heart mitochondrial monoamine oxidase (MAO) is activated by reserpine. So far activation of MAO by reserpine could only be demonstrated in vivo, or in slices in vitro. (2) When 14C-dopamine or 14C-tyramine, better substrates for mitochondrial MAO than norepinephrine, were used as substrates for MAO activity, there was little increase in their deamination after reserpine-treatment. (3) Even when 14C-norepinephrine was used as a substrate for MAO, there was little or no increase in its deamination after reserpine treatment when measured in hypotonie medium. The increase seen with normal heart preparations was probably caused by swelling or structural changes of heart mitochondria leading to increased deamination of 14C-norepinephrine. (4) These findings suggest the interesting possibility that reserpine may act on the mitochondrial membrane or structure to increase the penetration of norepinephrine to mitochondrial MAO. In this way the deamination of norepinephrine would be increased in hearts after reserpine treatment. © 1969.