Biosynthesis of 18-hydroxycorticosterone and aldosterone from corticosterone by bovine, guinea pig, and particularly sheep adrenal tissue has been studied. Both "18-hydroxylase" and "18-ol-dehydrogenase" were located mainly in the mitochondrial fraction.Reduced triphosphopyridine nucleotide (TPNH)and not reduced diphosphopyridine nucleotide (DPNH) was the cofactor for C-18 hydroxylation; presence of oxidized triphosphopyridine (TPN+) or diphosphopyridine nucleotide (DPN +) in the incubation media resulted in the conversion of 18-hydroxycorticosterone into 18-hydroxy-11 -dehydrocorticosterone and not into aldosterone. Ca2+ stimulated the conversion of corticosterone into 18-hydroxycorticosterone. SU 4885 [ 1,2-bis(3-pyridyl)-2-methyl-1 -propanone] and SU 9055 [3-(l ,2,3,4-tetrahydr-1 -oxo-2-naphthyl)pyri-P JL rogesterone, 11-deoxycorticosterone,* 1 *and corticosterone have been shown to be precursors of aldosterone biosynthesis (

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The synthesis of two [14C] labelled compounds, dexclamol and butaclamol hydrochloride, having the octahydrobenzocyclohepta pyridoisoquinoline structure is described. Both compounds were prepared by the same synthetic route starting from silver [14C]‐cyanide and were labelled in the 14‐position. Butaclamol (specific activity 1.23 mCi/mmole) was obtained in 13% overall yield while dexclamol (specific activity 17.8 mCi/mmole), an optically active compound requiring resolution in its preparation, was obtained in 2% overall yield.