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1 Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Maryland
A series of sympathomimetic amines was found to have a wide range of activity in depleting endogenous and radioactive norepinephrine from the rat heart.
Tyramine releases H3-norepinephrine which has been recently bound to a greater degree than H3-norepinephrine which has been present in the heart for a longer period of time. The specific activity of depleted norepinephrine is different from that of the amine which remains in the heart. The tyramine-releasable store was calculated to have a half-life of several hours, while the tyramine-resistant store had a half-life of about 1 day. In contrast, the specific activity of norepinephrine depleted by reserpine is the same as that which remains in the heart.
The monoamine oxidase inhibitor, JB-516, partially blocked depletion of norepinephrine by reserpine, guanethidine and 
-methyl-meta-tyrosine, but not the release by amphetamine. These results support the concept that reserpine and guanethidine release norepinephrine which is largely metabolized intraneuronally by monoamine oxidase, whereas sympathomimetic amines act upon another store to release norepinephrine from the nerve which is metabolized by catechol-O-methyl transferase. Bretylium was found to block partially the depleting actions of reserpine and guanethidine, but not the release by amphetamine or -methyl-meta-tyrosine. Cocaine blocked norepinephrine depletion by tyramine.
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