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(Circulation. 1998;97:292-293.)
© 1998 American Heart Association, Inc.

Correspondence

Vasopressin Deficiency and Vasodilation of Septic Shock

Steven R. Goldsmith, MD

Chief, Cardiology Division, Hennepin County Medical Center, Professor of Medicine, University of Minnesota Medical School, Minneapolis, Minn

To the Editor:

The article by Landry et al entitled "Vasopressin Deficiency Contributes to the Vasodilation of Septic Shock" (Circulation. 1997;95:1122–1125) is original and provocative in its findings of apparently low plasma vasopressin concentration in septic shock, coupled with the observation that infusion of vasopressin rapidly restored arterial pressure. Two points can be made regarding the conclusions and subsequent speculation about the reason for low vasopressin levels in this setting. First, the data obviously do not establish an actual contributing role for diminished arginine vasopressin levels in the hypotension of the syndrome, only that levels are low and infusion of vasopressin restores blood pressure. This observation may have therapeutic, not mechanistic, implications because, as noted by Dr Reid in the accompanying editorial, infusion of other peptides might have had similar effects. Second, although autonomic or baroreceptor dysfunction is postulated to account for the low arginine vasopressin levels, the explanation may in fact be due to the hemodynamics of septic shock coupled with normal baroreflex function. The sinoaortic baroreceptor is the dominant component of the afferent limb for nonosmotic arginine vasopressin secretion in humans.¹ These receptors respond to stretch, and pulsatile load may be a factor in governing their discharge frequency,² although mean arterial pressure is frequently the only variable cited. There is evidence that pulsatile load, especially at lower pressures, is associated with greater inhibitory effects on sympathetic activity than comparable levels of pressure with a static load³ ; the same physiology may well apply for vasopressin secretion, . . . [Full Text of this Article]

Juan A. Oliver, MD; ; Donald W. Landry, MD, PhD

Division of Nephrology, Columbia University, New York, NY