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(Hypertension. 2007;49:e32.)
© 2007 American Heart Association, Inc.
Letters to the Editor |
Autonomic Dysfunction Center, Division of Clinical Pharmacology, Departments of Medicine and Pharmacology, Vanderbilt University School of Medicine, Nashville, Tenn
Autonomic Dysfunction Center, Division of Clinical Pharmacology, Departments of Medicine, Pharmacology, and Neurology, Vanderbilt University School of Medicine, Nashville, Tenn
Ferreira-Filho et al1 are to be commended for their work assessing the hemodynamic impact of food and water. We can attest to the difficulties involved in conducting careful patient-oriented investigations as they have done in this research letter. They note that whereas water had a pressor response in their patients, food intake caused postprandial hypotension. They speculate that if they were taken together, then food intake might diminish (or eliminate) the pressor response of water. We agree fully with this statement, and the mechanism may relate to a "decrease in the hypo-osmolality" of water that we think might be a part of the signaling for this gastropressor response.2
In addition, the authors suggest that water might also be an effective treatment for postprandial hypotension. This is an exciting hypothesis that requires further testing. Postprandial hypotension can be a debilitating condition, and the mechanisms of this hypotension are not clear.3 Possibilities include a diversion of blood from the systemic to the splanchnic circulation with meals,4 or, alternatively, the hypotension could result from vasodilation resulting from the food-induced release of insulin.5 Current treatments can be expensive and sometimes require injectable peptides, such as somatostatin analogues.6 If "plain old water" can be shown to be an effective treatment of postprandial hypotension, this will represent a significant advance in the clinical care of this patient population. We hope that the authors will be conducting follow-up studies to determine whether this is indeed the case.
| Acknowledgments |
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Supported in part by National Institutes of Health grants 2P01 HL071784, K23 RR020783, M01 RR00095 (General Clinical Research Center).
Disclosures
None.
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