The accumulation and metabolism of exogenously administered 3H-epinephrine in the hearts of hypophysectomized and adrenalectomized rats were studied. Glucocorticoid biosynthesis in vivo was also inhibited with administration of 50 mg of metopirone or 25 mg of elipten, and metabolic fate of 3H-epinephrine in the heart was determined. All the above pharmacological or surgical manipulations employed to suppress adrenocortical function resulted in marked and highly significant decreases in the accumulation of 3H-epinephrine in the rat heart. The administration of ACTH to hypophysectomized rats increased significantly the retention of 3H-epinephrine and brought back to the level of non-hypophysectomized controls. The compensation of adrenalectomized rats with hydrocortisone also produced in creased accumulation of 3H-epinephrine in the heart. The rate of metabolism of tritiated epinephrine to tritiated acid metabolites and metanephrine was at the highest level in the hypophysectomized rats. The effects of adrenalectomy and glucocorticoid inhibition with metopirone or elipten produced only slight variations in the conversion of 3H-epinephrine to 3H-metanephrine and 3H-acid metabolites. The results provide evidence that the normal concentrations of adrenal cortical steroids are essential for the normal uptake of catecholamines by the heart. The results also suggest that adrenocortical hormones inhibit metabolism of exogenously administered 3H-epinephrine. The inactivation of adrenal steroidogenesis results in significant increases in catecholamine metabolite formation.

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