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Adrenergic Modulation of Adrenocorticotropin Responses to Insulin-Induced Hypoglycemia and Corticotropin-Releasing Hormone^*

Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College Tokyo, Japan

Address requests for reprints to: Naoki Tomori, M.D., Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, 8–1 Kawada-cho, Shinjuku-ku, Tokyo 162, Japan.

To study possible adrenergic modulation of pituitary- adrenal responses to insulin-induced hypoglycemia and CRH we examined the effect of nonselective β-blockade (phentolamine) and nonselective β-blockade (propranolol) on plasma ACTH, cortisol, and vasopressin (AVP) responses to hypoglycemia and CRH in five normal men.

Infusion of propranolol or phentolamine did not alter basal plasma ACTH or cortisol levels. The propranolol infusion enhanced the stimulatory effect of hypoglycemia on ACTH, cortisol, and AVP secretion and also enhanced the stimulatory effect of CRH on ACTH and cortisol secretion. Infusion of phentolamine inhibited hypoglycemia-induced ACTH and AVP secretion, but had no effect on the stimulatory effect of CRH on ACTH and cortisol secretion.

The increments of plasma ACTH and cortisol induced by an almost maximal dose of CRH (1 µg/kg) were smaller than those induced by hypoglycemia. The propranolol-induced enhancement of the ACTH response to hypoglycemia was almost the same as the ACTH response to CRH alone. From these results we conclude that propranolol may act at the pituitary level to enhance CRH action, rather than AVP action, and that the ACTH response to hypoglycemia may be mediated by hypothalamic -adrenergic activation.

^* This work was supported in part by a research grant from the Japanese Ministry of Education, Science, and Culture and a Research Grant for Intractable Disease from the Japanese Ministry of Health and Welfare.

Received March 7, 1988.