False Transmitters as Antihypertensive Agents

  • C. C. Porter
  • M. L. Torchiana
  • C. A. Stone
Part of the Handbuch der experimentellen Pharmakologie / Handbook of Experimental Pharmacology book series (HEP, volume 39)

Abstract

Early in the 1960’s, it became apparent that the known ability of α-methyl aromatic amino acids to inhibit aromatic amino acid decarboxylation (Sourkes, 1954; Westerman, Balzer, and Knell, 1958; Denglerand Reichel, 1958; Smith, 1960) was not solely responsible for the depression of biogenic amine concentrations in tissues following the administration of α-methyldopa or α-methyl-m-tyrosine to animals. Norepinephrine concentrations in the tissues of animals which received the amino acids returned to normal considerably more slowly than serotonin and dopamine concentrations (Hess et al., 1961; Porteret al., 1961; Stone et al., 1961), and considerably more potent decarboxylation inhibitors had little effect upon tissue catecholamine concentrations (Udenfriend and Zaltzman-Nlrenberg, 1962).

Keywords

Cocaine Clonidine Ouabain Methamphetamine Guanethidine 

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© Springer-Verlag Berlin · Heidelberg 1977

Authors and Affiliations

  • C. C. Porter
  • M. L. Torchiana
  • C. A. Stone

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