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

From the Department of Neurology (Drs. Lipp, Tank, and Arnold), Medical University Charité, and the Franz-Volhard Clinical Research Center (Drs. Luft and Jordan, G. Franke), Medical Faculty of the Charité and Helios Klinikum, Berlin, Germany.

Address correspondence and reprint requests to Dr. Jens Jordan, Franz-Volhard Clinical Research Center, Haus 129, Wiltbergstrasse 50, D-13125 Berlin, Germany; e-mail: jordan{at}fvk.charite-buch.de

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.

Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the September 27 issue to find the title link for this article.

Disclosure: The authors report no conflicts of interest.

Received March 28, 2005. Accepted in final form June 10, 2005.

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