McHugh and colleagues found that water introduced directly into the stomach or duodenum (the first part of the small intestine) raised blood pressure, which ruled out an oral or esophageal mechanism for the response. They also tested a similar volume of saline (salt-containing solution). This did not raise blood pressure, which suggested that stretch of the tissues was not part of the mechanism and that perhaps water's lack of salt might be important.
The investigators ultimately determined that water dilutes the plasma in the blood vessels leading away from the duodenum and that this short-lived reduction in salt concentration (hypo-osmolality) is responsible for water's blood pressure-raising (pressor) effect. They implicated a protein called Trpv4 in the mechanism: mice lacking the Trpv4 gene did not have a pressor response to water.
While it is clear that water evokes a pressor response, the normal role for this physiological system is not certain.
Because it raises sympathetic nervous system activity and consequently energy expenditure it does promote weight loss, Robertson said.
"I calculated it might be as much as five pounds a year if you drank three 16 ounce glasses of water a day and nothing else changed. This is not going to be the answer to the weight problem in the United States, but it's interesting that activation of the sympathetic system is enough to do that."
McHugh said she found it fascinating that mice and humans share "such a primitive system, and yet we don't know why it's there or what beneficial effects it might have."
The newly discovered system and its molecular mediators such as Trpv4 may be targets for blood pressure regulation, particularly in
|Contact: Leigh MacMillan|
Vanderbilt University Medical Center