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Research Article Free access | 10.1172/JCI105504

Increased Plasma Arginine Vasopressin in Clinical Adrenocortical Insufficiency and Its Inhibition By Glucosteroids

Abdul B. J. Ahmed, Barbara C. George, Carlos Gonzalez-Auvert, and Joseph F. Dingman

Lahey Clinic Foundation Endocrine Research Unit, Robert B. Brigham Hospital, and the Department of Medicine, Peter Bent Brigham Hospital and Harvard Medical School, Boston, Mass.

†

Address requests for reprints to Dr. Joseph F. Dingman, Peter Bent Brigham Hospital, 721 Huntington Ave., Boston, Mass. 02115.

*

Submitted for publication February 4, 1966; accepted September 28, 1966.

Supported in part by U. S. Public Health Service grants HE06965 and AM05577.

Dedicated to Dr. George W. Thorn on his sixtieth birthday.

A preliminary report of this work has been published in abstract form (1).

Find articles by Ahmed, A. in: JCI | PubMed | Google Scholar

Lahey Clinic Foundation Endocrine Research Unit, Robert B. Brigham Hospital, and the Department of Medicine, Peter Bent Brigham Hospital and Harvard Medical School, Boston, Mass.

†

Address requests for reprints to Dr. Joseph F. Dingman, Peter Bent Brigham Hospital, 721 Huntington Ave., Boston, Mass. 02115.

*

Submitted for publication February 4, 1966; accepted September 28, 1966.

Supported in part by U. S. Public Health Service grants HE06965 and AM05577.

Dedicated to Dr. George W. Thorn on his sixtieth birthday.

A preliminary report of this work has been published in abstract form (1).

Find articles by George, B. in: JCI | PubMed | Google Scholar

Lahey Clinic Foundation Endocrine Research Unit, Robert B. Brigham Hospital, and the Department of Medicine, Peter Bent Brigham Hospital and Harvard Medical School, Boston, Mass.

†

Address requests for reprints to Dr. Joseph F. Dingman, Peter Bent Brigham Hospital, 721 Huntington Ave., Boston, Mass. 02115.

*

Submitted for publication February 4, 1966; accepted September 28, 1966.

Supported in part by U. S. Public Health Service grants HE06965 and AM05577.

Dedicated to Dr. George W. Thorn on his sixtieth birthday.

A preliminary report of this work has been published in abstract form (1).

Find articles by Gonzalez-Auvert, C. in: JCI | PubMed | Google Scholar

Lahey Clinic Foundation Endocrine Research Unit, Robert B. Brigham Hospital, and the Department of Medicine, Peter Bent Brigham Hospital and Harvard Medical School, Boston, Mass.

†

Address requests for reprints to Dr. Joseph F. Dingman, Peter Bent Brigham Hospital, 721 Huntington Ave., Boston, Mass. 02115.

*

Submitted for publication February 4, 1966; accepted September 28, 1966.

Supported in part by U. S. Public Health Service grants HE06965 and AM05577.

Dedicated to Dr. George W. Thorn on his sixtieth birthday.

A preliminary report of this work has been published in abstract form (1).

Find articles by Dingman, J. in: JCI | PubMed | Google Scholar

First published January 1, 1967 - More info

Published in Volume 46, Issue 1 on January 1, 1967
J Clin Invest. 1967;46(1):111–123. https://doi.org/10.1172/JCI105504.
Copyright © 1967, The American Society for Clinical Investigation.

First published January 1, 1967 - Version history
Abstract

Trichloroacetic acid extracts of plasma were fractionated on a CG-50 resin column and the 50% acetic acid eluents chromatographed on silicic acid-impregnated glass paper in butanol-acetic acid-water. The specific arginine vasopressin (AVP) zone was eluted and assayed for antidiuretic activity in the diuretic rat. Thioglycolate inactivation was used to confirm AVP activity. Recovery of as little as 4 μU AVP per ml plasma ranged between 80 and 90%. In normal subjects after an overnight fast, plasma AVP ranged between 2.5 and 10.0 μU per ml. AVP secretion was inhibited by hemodilution and stimulated with nicotine and hypertonic saline. Plasma AVP was absent in patients with diabetes insipidus even after neurohypophyseal stimulation. Plasma AVP was abnormally elevated during mild dehydration and remained above the normal range despite hemodilution in patients with untreated adrenocortical insufficiency demonstrating a delayed water diuresis. Glucosteroid therapy lowered plasma AVP to normal in dehydrated patients. A normal diuretic response to hydration was accompanied by a fall in plasma AVP to zero in steroid-treated patients. These findings suggest that hypersecretion of AVP may play an important role in the abnormal water metabolism of adrenocortical insufficiency and that the glucosteroids promote normal water diuresis by inhibiting the secretion of AVP from the neurohypophysis.

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Version history
  • Version 1 (January 1, 1967): No description
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