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Osmosensitive mechanisms contribute to the water drinking-induced pressor response in humans

Item Type:Article
Title:Osmosensitive mechanisms contribute to the water drinking-induced pressor response in humans
Creators Name:Lipp, A. and Tank, J. and Franke, G. and Arnold, G. and Luft, F.C. and Jordan, J.
Abstract:Background: Water drinking elicits a sympathetically mediated pressor response in multiple-system atrophy patients through an unknown mechanism. We reasoned that gastrointestinal distention, hyposomotic stimulation, or both contribute to the water-induced pressor response Methods: We compared the response to normal saline and water on blood pressure in 10 patients with probable multiple-system atrophy. Patients featured moderate to severe autonomic dysfunction. EKG and finger arterial blood pressure were recorded continuously, and 500 mL normal saline and distilled water were each given in a single-blinded fashion. Fluids were applied through a previously inserted nasogastric tube within a 5-minute period. Results: Blood pressure began to increase within 10 minutes after water administration and reached a maximum after 20 minutes. Blood pressure did not change after saline administration. The blood pressure change after 20 minutes was 8 ± 9/2 ± 5 mmHg with water and –1 ± 11/–1 ± 7 mmHg with normal saline administration (p = 0.02 between interventions). Heart rate did not change with either intervention. Conclusion: Ingestion of water elicits a greater pressor response than the ingestion of normal saline. Thus, gastric distention is probably not the crucial mechanisms for the water-induced pressor response. Instead, the response may be mediated through osmosensitive afferent structures in the gastrointestinal tract, portal vein, and liver.
Keywords:Autonomic Nervous System Diseases, Blood Pressure, Drinking, Gastrointestinal Tract, Liver, Multiple System Atrophy, Neurological Models, Portal Vein, Sodium Chloride, Vasoconstriction, Visceral Afferents, Water, Water-Electrolyte Balance
Source:Neurology
ISSN:0028-3878
Publisher:American Academy of Neurology (U.S.A.)
Volume:65
Page Range:905-907
Date:27 September 2005
Official Publication:https://doi.org/10.1212/01.wnl.0000176060.90959.36
PubMed:View item in PubMed

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