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1 Laboratory of Clinical Biochemistry and the Experimental Therapeutics Branch, National Heart Institute, National Institutes of Health, Bethesda, Maryland
When rats were exercised or exposed to cold, the levels of norepinephrine in heart, spleen and brain showed little change. Appreciable decreases were observed in adrenal epinephrine following severe exercise. However, when the tyrosine hydroxylase inhibitor, 
-methyl-tyrosine, was administered prior to the exercise or exposure to cold, norepinephrine and epinephrine levels fell markedly in most tissues. Furthermore, incorporation of radioactivity from administered tyrosine-C14 into norepinephrine and epinephrine was increased 2-to 3-fold as a result of exercise. These findings indicate that the increased sympathetic stimulation, presumably associated with such stressful conditions, induces increased synthesis of norepinephrine and epinephrine. The regulatory mechanism most likely operates at the tyrosine hydroxylase step, which is ratelimiting.
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