THE DEPLETION OF CARDIAC NOREPINEPHRINE BY 3,5-DIHYDROXY-4-METHOXYPHENETHYLAMINE AND RELATED COMPOUNDS

¹ Laboratory of Chemistry, National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Maryland

A comparison was made of the ability of phenolic phenethylamines and their O-methyl congeners to deplete both prelabeled cardiac H³-norepinephrine and endogenous norepinephrine stores in the mouse. O-methyl derivatives were inactive with the notable exception of 3,5-dihydroxy-4-methoxyphenethylamine, which proved to be an effective releasing agent. The ED50 of this amine, the -hydroxylated analog and 3,4,5-trihydroxyphenethylamine was determined and compared to reserpine, l-metaraminol, 6-OH dopamine and tyramine. The effects of cocaine and bretylium on the release of norepinephrine induced by these trioxy amines were determined. The metabolism of H³-norepinephrine in the isolated perfused rat heart during release with 3,5-dihydroxy-4-methoxyphenethylamine was compared to the metabolism obtained with reserpine and tyramine perfusion. A shift toward metabolism by monoamine oxidase was observed and a marked increase in the release of free catecholamine. Evidence is presented showing that 3, 5-dihydroxy-4-methoxyphenethylamine was taken up by the heart and converted to the -hydroxylated analog in vivo; also, this amine was shown to be a substrate for dopamine- hydroxylase in vitro.

This article has been cited by other articles:

				A. Sandrock Jr and W. Matthew An in vitro neurite-promoting antigen functions in axonal regeneration in vivo Science, September 25, 1987; 237(4822): 1605 - 1608. [Abstract] [PDF]