WILLIAM M. SMITH, M.D., F.A.C.P.; BRUCE BACHMAN, M.D.; JAMES G. GALANTE, M.D.; ERNEST G. HANOWELL, M.D., F.A.C.P.; WILLARD P. JOHNSON, M.D.; CHARLES E. KOCH JR., M.D.; STANLEY D. KORFMACHER, M.D.; RICHARD H. THURM, M.D., F.A.C.P.; LOUIS BROMER, B.A.
Alpha-methyldopa (alpha-methyl-3,4-dihydroxy-L-phenylalanine) has been shown to inhibit the decarboxylation of aromatic L-amino acids and to deplete tissue stores of norepinephrine. The studies of Sjoerdsma, Vendsalu, and Engelman (1) have shown that these two properties are clearly dissociable. Available evidence indicates that the hypotensive action of alpha-methyldopa is not via decarboxylation inhibition but rather is mediated by amine metabolites of the compound itself, such as alpha-methyldopamine and alpha-methylnorepinephrine. These are formed after its decarboxylation and may function as "false transmitters," competing with norepinephrine for storage sites, from which they may be poorly released or less effective or both (2). Numerous investigators
SMITH WM, BACHMAN B, GALANTE JG, HANOWELL EG, JOHNSON WP, KOCH CE, et al. Co-operative Clinical Trial of Alpha-methyldopa: III. Double-blind Control Comparison of Alpha-methyldopa and Chlorothiazide, and Chlorothiazide and Rauwolfia. Ann Intern Med. 1966;65:657–671. doi: 10.7326/0003-4819-65-4-657
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Published: Ann Intern Med. 1966;65(4):657-671.
Cardiology, Coronary Risk Factors, Hematology/Oncology, Hospital Medicine, Hypertension.
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