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THE rauwolfia alkaloids have been widely used in clinical practice, but relatively little information concerning the mechanism of their circulatory action in man is available. Reserpine has been extensively studied in laboratory animals, and it has been demonstrated that after the parenteral administration of relatively large doses of this drug, postganglionic sympathetic nerves are no longer able to transmit impulses across the neuroeffector junctions.1 Also, in animals, a profound fall in the concentration of norepinephrine, epinephrine and serotonin throughout the body occurs after reserpine administration,2 3 4 and the sympathetic blockade produced by reserpine in laboratory animals has been attributed to the . . .
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Charles A. Chidsey
National Institutes of Health
Eugene Braunwald
Boston University
Andrew G. Morrow
Newark Beth Israel Medical Center
New England Journal of Medicine
National Heart Institute
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Chidsey et al. (Thu,) studied this question.
synapsesocial.com/papers/6a20a288239b4646016d917a — DOI: https://doi.org/10.1056/nejm196309262691302