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Atrial Natriuretic Polypeptide Inhibits Cortisol Secretion as Well as Aldosterone Secretion in Vitro from Human Adrenal Tissue^*

Institute of Clinical Endocrinology, Department of Medicine, Tokyo Women’s Medical College Tokyo 162
Department of Medicine, Iwaki-kyoritsu General Hospital Iwaki, Fukushima 973, Japan
The Department of Biochemistry and Hypertension Center, Vanderbilt University Nashville, Tennessee 37232

Address requests for reprints to: Dr. Mitsuhide Naruse, Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women’s Medical College, Tokyo 162, Japan.

The effect of -human atrial natriuretic poly-peptide (ANP) on adrenal steroidogenesis was studied in human adrenal tissues obtained surgically from four patients with Cushing’s syndrome due to an adrenal adenoma and five patients with an aldosterone-producing adenoma (APA). ANP significantly inhibited basal and ACTH (3.4 x 10^–8 M)-stimulated cortisol and aldosterone secretion in both the adenomas and adjacent adrenocortical tissues from patients with Cushing’s syndrome. ANP inhibited ACTH-stimulated, but not basal, secretion of cortisol and aldosterone in the adjacent tissues from patients with APA. In addition, ANP significantly inhibited both basal and ACTH-, angiotensin II (10^–6 M)-, and potassium chloride (10 mM)-stimulated secretion of aldosterone from the adenomas of patients with APA. ANP-induced changes in cortisol and aldosterone secretion were accompanied by a decrease in cAMP and an increase in cGMP secretion. These results suggest that ANP may be a possible regulator of cortisol as well as aldosterone secretion in humans, and these effects might be due to concomitant alteration in cyclic nucleotide metabolism.

^* This work was supported in part by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science, and Culture (Japan); a research grant from the Intractable Diseases Division, Japanese Ministry of Health and Welfare; and research grants from the Foundation for Growth Science in Japan and the NIH (HL-14192).

Received April 23, 1986.

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