Abstract
The fate of norepinephrine-H3 has been investigated in the isolated perfused hearts of normal and reserpine pretreated rats. In normal hearts norepinephrine is inactivated primarily by binding. In perfused hearts from normal rats, O-methylation is the predominant pathway of metabolic inactivation. Reserpinized hearts have a decreased binding capacity, but a greater proportion of the infused norepinephrine is metabolized. The increase in metabolic products in the reserpinized hearts is confined to the deaminated catechols and their O-methylated derivatives. The presence of several types of binding is indicated by the observed multiphasic release of bound norepinephrine. It is suggested that the free, active, and easily released norepinephrine is metabolized by O-methylation, while the more firmly bound, reserpine depleted norepinephrine is deaminated without becoming active.
Footnotes
- Received June 23, 1962.
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