The effects of hydrocortisone (2.5 ×10–8M) on accumulation and metabolism of 14C-norepinephrine (14C-NE) by isolated rabbit aorta have been studied over a 2-hour period. 14C-NE and metabolites were isolated from tissue homogenates by means of column chromatography. Hydrocortisone significantly reduced uptake of 14C-NE after 40 min. o-Methylated 14C-NE metabolites were also significantly reduced and no 14C-dihydroxymandelic acid was recovered from tissue homogenates. It appears that hydrocortisone may impede transmembrane movements of 14C-NE to sites of enzymatic inactivation in vascular smooth muscle. Further studies were conducted to compare the effects of a catechol-o-methyltransferase inhibitor (3’,4’-dihydroxy-2-methylpropiophenone, U-0521) and a monoamine oxidase inhibitor (iproniazid) with those of hydrocortisone, desoxycorticosterone acetate and progesterone on initial accumulation and metabolism of 14C-NE by aortae after 10 min exposure to 14C-NE. U-0521, desoxycorticosterone acetate and progesterone significantly reduced 14C-NE accumulation by aortae. All three steroids significantly reduced the amount of o-methylated and deaminated 14C-NE metabolites recovered from aortae. The amount of unmetabolized 14C-NE recovered was not altered by the steroids. Therefore, it appears that all the steroids tested have the ability to limit the transmembrane movements of 14C-NE in vascular smooth muscle which are necessary for enzymatic destruction. This effect may account for the ability of steroid hormones to potentiate catecholamine-induced contraction in vascular smooth muscle.

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