To the Editor.
—In the September Archives, Sigman and Wallach1 described a patient with unilateral adrenal hypertrophy and contralateral adrenal atrophy. The authors suggested this was the result of an invasive metastasis to the hypertrophic adrenal that produced ACTH and consequently through hypothalamic feedback caused the contralateral adrenal atrophy. The authors stated since circulating plasma ACTH levels were elevated, bilateral adrenal hypertrophy would be expected.Recently, animal studies have implicated direct autonomic regulation of adrenal corticol sensitivity to ACTH. To illustrate, Meier2 has shown that hypophysectomized rats still exhibit a circadian rhythm of plasma corticosteroid with implant replacement of ACTH and thyroxine. Hence, cyclic variations in plasma corticosteroids occurred in the absence of cyclic pituitary output. These daily variations are abolished by transecting the splanchnic nerve trunks to the adrenals.3 In addition, Engeland and Dallman4 have shown that transection of the splanchnic nerves to the adrenals