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The Journal of Clinical Endocrinology & Metabolism Vol. 86, No. 12 5749-5754
Copyright © 2001 by The Endocrine Society


Other Original Articles

Increases in Plasma ACTH and Cortisol after Hypertonic Saline Infusion in Patients with Central Diabetes Insipidus

Eiji Itagaki, Sachihiko Ozawa, Shinya Yamaguchi, Kenji Ushikawa, Teruaki Tashiro, Hiroshi Katahira, Makoto Takizawa, Katsuhiko Yoshimoto, Shoichiro Murakawa and Hitoshi Ishida

Third Department of Internal Medicine, Kyorin University School of Medicine, Mitaka, Tokyo 181-8611, Japan

Address all correspondence and requests for reprints to: Eiji Itagaki, M.D., Ph.D., Third Department of Internal Medicine, Kyorin University School of Medicine, 6-20-2 Shinkawa, Mitaka, Tokyo 181-8611, Japan. E-mail: ita{at}kyorin-u.ac.jp

Abstract

To clarify the mechanism for the potentiation of CRH-induced ACTH response by the infusion of hypertonic saline, we investigated changes in plasma ACTH concentration after infusion of 5% hypertonic saline in five patients with untreated central diabetes insipidus (DI). Basal levels of plasma ACTH and cortisol in the DI group were not significantly different from those in normal control subjects. The infusion of hypertonic saline produced an increase in plasma arginine vasopressin (AVP) in controls, but did not elevate ACTH. However, in patients with DI, the plasma AVP concentration did not change, but circulating ACTH increased 3.6-fold (7.7 ± 1.5 to 23.0 ± 2.7 pmol/liter; P < 0.01), and plasma cortisol also increased significantly (298 ± 99 to 538 ± 124 nmol/liter; P < 0.05). Moreover, a positive correlation was observed between plasma ACTH and osmolality (r = 0.72; P < 0.005). These results indicate that ACTH secretion in DI patients is regulated by a mechanism distinct from that in healthy subjects. It seems possible that the increase in plasma osmolality promotes ACTH secretion in DI patients through AVP and/or urocortin via the hypophyseal portal system, independent of the AVP secretion from magnocellular neurons.







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Copyright © 2001 by The Endocrine Society