The nmr kinetic method has been extensively used for the measurement of barriers to internal rotation,6 and in some cases7-13 (see Discussion) it has been possible to determine the barrier as a function of substituent "size" for a limited number of substituents.In the 1,3,5-trineopentylbenzene series 1, we have available a molecular system in which barriers of the same group (tert-butyl) past the substituents H, F, Cl, Br, I, and CHS could be determined. We have previously reported the determination (by complete lineshape analysis) of barriers past chlorine,14•15 bro-

In order to test for dopamine-receptor stimulating activity a new, sensitive biochemical screening method was designed. For behavioral studies and for determination of the duration of action on the compounds, motor activity measurements were used. O,O'-Dipivaloyl-N,N-dipropyldopamine (4) was the only derivative of a series of dipivaloyl-N,N-dialkyldopamines studied that showed any significant activity. However, the monopivaloyl ester 2-(3-pivaloyloxyphenyl)-N,N-dipropylethylamine (8) seemed to be more potent. The same relationship was found for the corresponding phenols, N,N-dipropyldopamine (3) and 2-(3-hydroxyphenyl)-N,N-dipropylethylamine (7), although both were more active than their pivaloyl esters.

Coprine or disulfiram was given to rats in various doses at various time intervals before the administration of 2 g/kg ethanol. The ratio acetaldehyde/ethanol in the alveolar air was measured by gas chromatography and was taken as an index of the aldehyde dehydrogenase (ALDH) activity. The activity of dopamine β‐hydroxylase (DBH) was estimated in the same animals by measuring the amount of 14C‐octopamine formed from 14C‐tyramine in the heart. Coprine and disulfiram both caused an increase in the acetylaldehyde/ethanol ratio, coprine being more potent than disulfiram. Disulfiram, but not coprine, reduced the net yield of 14C‐octopamine. In rats pretreated with either coprine or disulfiram, blood‐pressure and heart‐rate were recorded before and after intraperitoneal injections of 0.4 g/kg ethanol. In both cases ethanol caused a marked and rapid fall in blood‐pressure. However, this effect was accompanied by tachycardia only in animals treated with coprine. It is concluded that coprine like disulfiram inhibits ALDH, but only disulfiram causes an additional inhibition of DBH. This difference may account for differences in the cardiovascular response to ethanol

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