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

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

doi: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

First published January 1, 1967 - More info

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.