Nonosmotic influences on osmotic stimulation of vasopressin in humans

Steven Goldsmith, D. Dodge, A. W. Cowley

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20 Scopus citations

Abstract

To study the influence of cardiopulmonary baroreceptor loading and unloading on the osmotic stimulation of arginine vasopressin (AVP) in normal humans, we gave 105-min 5% saline infusions (0.06 ml·kg-1·min-1) to three groups of subjects under different cardiopulmonary baroreceptor loading conditions. Group A received only the infusion, with a consequent increase in central venous pressure (CVP) of 2.6 ± 1.7 mmHg; group B had CVP held constant by continuous lower body negative pressure; and Group C had CVP decreased by -3.3 ± 1.4 mmHg, also with lower body negative pressure, for the duration of the infusion. Mean arterial pressure increased in group A by 6.6 ± 3.7 mmHg, but did not change in groups B and C. On average, osmolality increased by the same amount in each of the three groups (11.6 ± 3.3, 13.7 ± 3.2, and 10.9 ± 2.5 mosmol/kg, P = NS). The changes in AVP in the three groups were 3.6 ± 2.0, 2.7 ± 1.9, and 6.2 ± 3.5 pg/ml, P < 0.03, with group C different from group B and groups A and B not different by individual pairs testing. An independent effect of prolonged CVP reduction on AVP levels in group C was made unlikely by studies in four additional subjects in whom AVP did not change at constant osmolality during 105 min of CVP reduction comparable with that in group C. Thus modest loading of both cardiopulmonary and sinaortic baroreceptors does not alter the osmotic stimulation of AVP in normal humans. However, prolonged unloading of cardiopulmonary baroreceptors, although without effect on AVP levels if performed isosmotically, does appear to enhance the osmotic stimulation of AVP. These studies are consistent with a role for cardiopulmonary receptors in the regulation of AVP in humans, but one that may be limited to an interaction with the osmotic control system under unloaded conditions.

Original languageEnglish (US)
Pages (from-to)H85-H88
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume252
Issue number1 (21/1)
DOIs
StatePublished - 1987

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