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Journal of Pharmacology And Experimental Therapeutics, Vol. 169, Issue 2, 237-248, 1969
Copyright © 1969 by American Society for Pharmacology and Experimental Therapeutics

THE UPTAKE AND DISPOSITION OF dl-NOREPINEPHRINE IN PERFUSED RAT LUNG

JOHN HUGHES 1, C. N. GILLIS 1, and F. E. BLOOM 1

1 Department of Pharmacology, Yale University School of Medicine, New Haven, Connecticut

The fate of dl-norepinephrine-H3 (NE-H3) in lung was examined after perfusion of the amine through the rat lung in vitro. Lung tissues concentrated tritium after perfusion with NE-H3; however, chromatographic analysis showed that only 20% of retained radio-activity was due to unchanged NE, the remainder consisting of methylated and deaminated products. Treatment with both pargyline and tropolone significantly increased the total amount of tritium found in the lungs after perfusion with NE-H3 and increased to 97% the activity associated with unchanged amine. Uptake of NE-H3 was inhibited by cocaine. Experiments involving increasing concentrations of NE, perfused for 2, 5 or 10 minutes, showed that the uptake was saturable and had an apparent Km of 143 x 10-7 M and Vmax of 360 ng (215 x 10-3 mol) per mm per g. The uptake of epinephrine-H3 was qualitatively similar to that for NE-H3, but the process appeared to have a much greater affinity for NE-H3. The loss of accumulated radioactivity was examined in control lungs and in those exposed to pargyline and tropolone. The curves for loss of tritium from control lungs were best described by a three-exponential-component system, whereas the curves from drug-treated lungs could be fitted adequately by a two-component system. It was calculated that accumulated NE is distributed between two functionally distinct sites. Autoradiographic and electron microscope studies indicated that accumulation of NE occurred mainly in the peripheral portions of the vascular and respiratory system, possibly in both endothelial and adventitial surfaces of capillaries. It is proposed that capillary endothelial cells may be important sites for inactivation of circulating NE and that, in the lung, both monoamine oxidase and catechol-O-methyltransferase play significant roles in the overall inactivation process.

Submitted on January 20, 1969
Accepted on June 18, 1969




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