RT Journal Article
SR Electronic
T1 End-Product Inhibition of Tyrosine Hydroxylase as a Possible Mechanism for Regulation of Norepinephrine Synthesis
JF Molecular Pharmacology
JO Mol Pharmacol
FD American Society for Pharmacology and Experimental Therapeutics
SP 549
OP 555
VO 3
IS 6
A1 SPECTOR, SYDNEY
A1 GORDON, ROBERT
A1 SJOERDSMA, ALBERT
A1 UDENFRIEND, SIDNEY
YR 1967
UL http://molpharm.aspetjournals.org/content/3/6/549.abstract
AB 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.