Impaired response of plasma vasopressin to orthostatic stress in patients with congestive heart failure

Steven R. Goldsmith, Gary S Francis, T. Barry Levine, Allan W. Cowley, Jay N Cohn

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24 Scopus citations


Arginine vasopressin, a potent vasoconstrictor and regulator of body water, is frequently increased in the plasma of patients with congestive heart failure. Other neurohumoral control networks, such as the sympathetic nervous system and the renin-angiotensin system, also demonstrate increased activity in congestive heart failure, but fail to respond normally to physiologic stress, such as orthostatic tilt. To assess the response of plasma vasopressin to orthostasis in heart failure, vasopressin was measured before and at 10 and 45 minutes during passive upright tilt in 15 patients with congestive heart failure and their response was compared with that in 9 normal control subjects. Arginine vasopressin was measured by radioimmunoassay. In the normal subjects, plasma arginine vasopressin was 5.3 ± 2.3 pg/ml at control, was unchanged at 10 minutes, but significantly increased to 7.0 ± 2.5 pg/ml at 45 minutes (p < 0.05). In contrast, patients with congestive heart failure showed no significant changes in arginine vasopressin levels from the control levels of 11.6 ± 5.5 pg/ml. Both plasma norepinephrine and renin activity increased in the normal subjects, but failed to increase from higher baselines in patients with congestive heart failure. Thus, plasma arginine vasopressin, like plasma norepinephrine and renin activity, does not increase in response to upright tilt in patients with congestive heart failure. The explanation is not evident but could involve either abnormalities in reflex control of plasma vasopressin in congestive heart failure or in clearance of the hormone during orthostasis.

Original languageEnglish (US)
Pages (from-to)1080-1083
Number of pages4
JournalJournal of the American College of Cardiology
Issue number6
StatePublished - 1983

Bibliographical note

Funding Information:
From the Cardiovascular Division. University of Minnesota Medical School. Minneapolis. Minnesota and the Departmentof Physiology. Medical College of Wisconsm, Milwaukee. Wisconsin. Thrs research was supported m part by Trarrung Grant HL07184-06 and Research Grant HL22977-03 from the National Heart. Lung. and BloodInsntute. Bethesda, Maryland and by a Research Grant from the Veterans Adrmnistration, Washington.0 C.Dr.GoldsmithIStherecipientofaClinicalInvestigator Award from the National Heart, Lung. and Blood Insntute. Manuscript received March 21. 1983; revised manuscript received June 27. 1983. accepted July I. 1983.


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