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1 Department of Pharmacology and Neurology, College of Physicians and Surgeons of Columbia University, New York, and Laboratory of Chemical Pharmacology, National Heart Institute, National Institutes of Health, Bethesda, Maryland
In rats given 0.165 µg/kg of d,l-H3-NE or 0.165 µg/kg of l-H3-NE i.v., the labeled amine disappeared from the heart by a simple exponential decay, with a half-life of about 15 hr. After these small doses of H3-NE were given, the NE released by tyramine injection had the same specific activity as that remaining in the heart. When the dose of the labeled l-isomer or the racemate was increased to 2.16 µg/kg, the H3-NE in the heart was found to decline in two or more phases. These results suggest that the multiphasic decay curves for exogenous H3-NE do not reflect the behavior of the endogenous stores. Instead, the labeled amine, given in truly tracer doses that do not cause net accumulation of amine, appears to mix rapidly and uniformly with the NE stores in sympathetic nerve endings.
Submitted on October 13, 1967
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