MolPharm xPharm- The Comprehensive Pharmacology Reference

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by SPECTOR, S.
Right arrow Articles by UDENFRIEND, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by SPECTOR, S.
Right arrow Articles by UDENFRIEND, S.

Molecular Pharmacology, Vol 3, 549-555, Copyright © 1967 by the American Society for Pharmacology and Experimental Therapeutics

End-Product Inhibition of Tyrosine Hydroxylase as a Possible Mechanism for Regulation of Norepinephrine Synthesis

SYDNEY SPECTOR 1, ROBERT GORDON 1, ALBERT SJOERDSMA 1, and SIDNEY UDENFRIEND 1

1 Experimental Therapeutics Branch and the Laboratory of Clinical Biochemistry, National Heart Institute, National Institutes of Health, Bethesda, Maryland 20014

The present study was undertaken to evaluate the influence of endogenous norepinephrine content on the rate of norepinephrine synthesis in vivo. Tissue levels of norepinephrine were increased in guinea pigs by administration of a monoamine oxidase inhibitor and tyrosine-14C and DOPA-3H were used to measure norepinephrine synthesis. In brain and heart when norepinephrine levels were increased 2- to 3-fold, conversion of tyrosine-14C to norepinephrine was decreased markedly. When tyrosine hydroxylase was bypassed by administering DOPA-3H, conversion to norepinephrine was actually increased. These findings lend support to the hypothesis that norepinephrine synthesis is regulated by a mechanism of end-product inhibition at the tyrosine hydroxylase step.

Submitted on June 15, 1967




This article has been cited by other articles:


Home page
 J. Nutr.Home page
J. D. Fernstrom and M. H. Fernstrom
Tyrosine, Phenylalanine, and Catecholamine Synthesis and Function in the Brain
J. Nutr., June 1, 2007; 137(6): 1539S - 1547S.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
S. R. Jones, R. R. Gainetdinov, M. Jaber, B. Giros, R. M. Wightman, and M. G. Caron
Profound neuronal plasticity in response to inactivation of the dopamine transporter
PNAS, March 31, 1998; 95(7): 4029 - 4034.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
R. Betarbet, R. Turner., V. Chockkan, M. R. DeLong, K. A. Allers, J. Walters, A. I. Levey, and J. T. Greenamyre
Dopaminergic Neurons Intrinsic to the Primate Striatum
J. Neurosci., September 1, 1997; 17(17): 6761 - 6768.
[Abstract] [Full Text] [PDF]

Home page
 ScienceHome page
R. Denney, R. Fritz, N. Patel, and C. Abell
Human liver MAO-A and MAO-B separated by immunoaffinity chromatography with MAO-B-specific monoclonal antibody
Science, March 12, 1982; 215(4538): 1400 - 1403.
[Abstract] [PDF]

Home page
 ScienceHome page
J. J. Schildkraut, B. A. Keeler, M. Papousek, and E. Hartmann
MHPG Excretion in Depressive Disorders: Relation to Clinical Subtypes and Desynchronized Sleep
Science, August 24, 1973; 181(4101): 762 - 764.
[Abstract] [PDF]

Home page
 ScienceHome page
W. Dairman and S. Udenfriend
Decrease in Adrenal Tyrosine Hydroxylase and Increase in Norepinephrine Synthesis in Rats Given L-Dopa
Science, March 12, 1971; 171(3975): 1022 - 1024.
[Abstract] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
Molecular Interventions Drug Metabolism and Disposition

Copyright © 1967 by the American Society for Pharmacology and Experimental Therapeutics