Influence of the emetic reflex on vasopressin release in man

J. W. Rowe, R. L. Shelton, J. H. Helderman, R. E. Vestal, G. L. Robertson

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258 Scopus citations


The mechanisms underlying the frequent association of nausea and vomiting with elevations of plasma vasopressin (PAVP) were studied in man and rat. After oral water loads (N = 16), plasma osmolality fell in all human subjects and was associated with a decline in PAVP in 14 asymptomatic human subjects. In 2 human subjects, nausea occurred and was associated with increases in PAVP, without changes in blood pressure. During ethanol infusion (N = 28), PAVP was suppressed unless nausea supervened. In 4 nauseated human subjects, PAVP escaped from ethanol inhibition and rose to levels 10 times basal, despite the absence of hemodynamic changes. Apomorphine, a potent dopamine agonist and emetic agent, was administered to human volunteers in doses of 7 to 24 μg/kg. There was no increase in PAVP in 3 human subjects who remained asymptomatic (7 to 16 μg/kg). Ten human subjects experienced nausea after 16 μg/kg, which was followed shortly by marked increases in PAVP. Emesis occurred in 5 human subjects given 16 to 24 μg/kg, and was followed by PAVP levels similar to those seen with nausea alone. In 7 human subjects from the nausea group, the repeat study (16 μg/kg) after pretreatment with dopamine antagonist (haloperidol, N = 4; fluphenazine, N = 3) resulted in complete blockage of apomorphine-induced AVP release. In rats, which lack an emetic reflex, apomorphine in doses of 200 μg/kg induced only slight increases in PAVP when compared to the response to 16 μg/kg in man. These studies indicate that stimulation of the emetic reflex results in AVP-release in man. Nausea-mediated AVP release supervenes over concomitant osmolar or pharmacologic (ethanol) inhibition.

Original languageEnglish
Pages (from-to)729-735
Number of pages7
JournalKidney International
Issue number6
StatePublished - 1979
Externally publishedYes


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