Previous studies have shown on the basis of isolated omparisons that plasma arginine vasopressin (AVP) levels are inappropriately increased for a given serum osmolality in patients with CHF. To explore further the osmoregulation of AVP in this condition, the response of plasma AVP to a 15- to 20-ml/kg oral water load was compared in 26 patients with CHF and 14 normal subjects. In the normal subjects, serum osmolality decreased from 289 ± 5.0 to 282 ± 5.0 mOsm/kg (p < 0.001) and AVP from 3.6 ± 1.1 to 2.1 ± 0.78 pg/ml (p š 0.001). In the patients with CHF, osmolality decreased from 289 ± 7.0 to to 281 ± 7.0 mOsm/kg and AVP from 7.1 ± 3.6 to 5.8 ± 3.4 pg/ml (p < 0.001). As a percentage of the control value, the decrease in AVP was much greater in the normal group, 41 ± 15% vs 18 ± 10% (p < 0.001). Urinary osmolality levels were measured before and after water loading in 11 patients and in 7 normal subjects. Normal subjects diluted from 812 ± 130 to 133 ± 26 mOsm/kg (p < 0.001) and CHF patients from 599 ± 218 to 253 ± 170 mOsm/kg, a statistically significant (p < 0.01) but smaller (p < 0.05) level of suppression. There were, however, 2 distinct groups within the CHF population: one in which urine osmolality was appropriately decreased (from 594 ± 269 to 144 ± 37 mOsm/kg, p < 0.01) and one in which it decreased little (from 498 ± 84 to 443 ± 132 mOsm/kg, difference not significant). Changes in AVP during the tests were similar in the groups, and although the absolute levels were higher in the patients in whom dilution was abnormal, the minimum AVP level in the patients who diluted was still above normal (4.9 ± 1.8 pg/ ml). The data suggest a variable relation between AVP and urinary osmolality in patients with CHF. Persistently elevated AVP levels may be associated with either normal or abnormal urine dilution in such patients.
Bibliographical noteFunding Information:
From the Hennepin County and Veterans Administration Medical Centers, University of Minnesota School of ,Medicine, Minneapolis, Minnesota, and the Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin. This research was supported in part by Training Grant HL07184-06 and Research Grant HL22977-03 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland, and by a Research Grant from the Veterans Administration, Washington, D.C. Dr. Goldsmith is recipient of a Clinical Investigator Award from the National Heart, Lung, and Blood Institute. Manuscript received January 13, 1986; revised manuscript received March 27, 1986, accepted March 31,1986. Address for reprints: Steven R. Goldsmith, MD, Hennepin County Medical Center, Cardiology Section, 701 Park Avenue South, Minneapolis, Minnesota 55415.