Baroreceptor-mediated suppression of osmotically stimulated vasopressin in normal humans

Steven Goldsmith

Research output: Contribution to journalArticlepeer-review

23 Scopus citations

Abstract

Increases in central venous pressure and arterial pressure have been reported to have variable effects on normal arginine vasopressin (AVP) levels in healthy humans. To test the hypothesis that baroreceptor suppression of AVP secretion might be more likely if AVP were subjected to a prior osmotic stimulus, we investigated the response of plasma AVP to increased central venous pressure and mean arterial pressure after hypertonic saline in six normal volunteers. Plasma AVP, serum osmolality, heart rate, central venous pressure, mean arterial pressure, and pulse pressure were assessed before and after a 0.06 ml·kg-1·min-1-infusion of 5% saline give over 90 min and then after 10 min of 30° head-down tilt and 10 min of head-down tilt plus lower-body positive pressure. Hypertonic saline increased plasma AVP. After head-down tilt, which did not change heart rate, pulse pressure, or mean arterial pressure but did increase central venous pressure, plasma AVP fell. Heart rate, pulse pressure, and central venous pressure were unchanged from head-down tilt values during lower-body positive pressure, whereas mean arterial pressure increased. Plasma AVP during lower-body positive pressure was not different from that during tilt. Osmolality increased during the saline infusion but was stable throughout the remainder of the study. These data therefore suggest that an osmotically stimulated plasma AVP level can be suppressed by baroreflex activation. Either the low-pressure cardiopulmonary receptors (subjected to a rise in central venous pressure during head-down tilt) or the sinoaortic baroreceptors (subjected to hydrostatic effects during dead-down tilt) could have been responsible for the suppression of AVP. AVP levels did not, however, decline further in response to the increased mean arterial pressure caused by the lower-body positive pressure. Further delineation of the exact nature of the variables responsible for the suppression of AVP during head-down tilt and of the effects of an isolated rise in arterial pressure require further study.

Original languageEnglish (US)
Pages (from-to)1226-1230
Number of pages5
JournalJournal of applied physiology
Volume65
Issue number3
StatePublished - Jan 1 1988

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