Fate of H³-noradrenaline in skeletal muscle before and following sympathetic stimulation

¹ Laboratory of Clinical Science, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland

The vascular bed of dog musculus gracilis in situ was perfused with blood at a constant flow rate. Infused H³-noradrenaline was retained and then released spontaneously at a slow rate. The major fraction of released radioactivity has been identified as normetanephrine, 3-methoxy-4-hydroxymandelic acid, and 3-methoxy-4-hydroxyphenylglycol. Upon vasomotor nerve stimulation, there was a concomitant reduction in outflow of total radioactivity and in noradrenaline metabolites and delayed elevation of noradrenaline outflow. After cessation of the stimulus, return of peripheral resistance and decline in noradrenaline outflow were parallel. Vasomotor nerve stimulation after pretreatment with phenoxybenzamine resulted in an immediate and larger increase in noradrenaline outflow. Vasomotor nerve stimulation did not induce any net change in the outflow of metabolic products. Rebinding of liberated noradrenaline and diffusion and removal by the circulation appear to be the major mechanisms for ending the action of noradrenaline. Transcapillary transport is reduced by the liberated noradrenaline and this serves to prolong the action of the neurohumor.

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