Abstract

Water ingestion induces a robust, sustained pressor response in patients with baroreflex impairment and in mice with sinoaortic deafferentation (SAD). The mechanism of water's effect on blood pressure remains unknown. In order to isolate the location at which water acts, SAD mice were given water via intragastric or intraduodenal routes. In both cases a similar pressor response appeared. The presence of a pressor response following intraduodenal infusion indicates that the pharynx, esophagus, and stomach are not critical sites for water's pressor action. Administering an identical volume of physiological saline did not induce a significant pressor response. Osmolality of portal and systemic circulations was measured 15 minutes post intraduodenal water infusion and found to be 292.7 and 304.4 mOsm/kg, respectively. TRPV4 is an osmo‐sensitive cation channel found throughout the body, and has been reported to be activated under hypotonic conditions. To investigate the potential role of TRPV4 in water's pressor response, animals lacking TRPV4 were given water intraduodenally. Compared to wild type, TRPV4 ‐/‐ animals had a greatly diminished pressor response to water. We conclude that the pressor effect of water is not dependent on pharyngeal, esophageal, nor gastric mechanisms; portal osmolality is reduced following water administration; and that the TRPV4 channel is essential for water's effect.

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