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Jonathan Williams, M.D.
Diastolic dysfunction is a cause of significant morbidity and mortality affecting approximately 5 million individuals in the United States. Relatively little is known about the pathophysiology of this condition leading to mostly empiric treatment with modest impact. We have shown that dietary sodium intake appears to modify normal diastolic function in humans and the mechanism responsible for this altered response is angiotensin II. These fundamental studies in normal volunteers raise the intriguing possibility that a dysfunctional response might be present in individuals with diastolic dysfunction thus resulting in an inability to respond appropriately to the high dietary sodium content of most Westernized diets. Planned studies will further delineate the role of angiotensin II in normal physiology, explore the relationship to central aortic stiffness, and finally investigate abnormal response characteristics in disease states (hypertensive heart disease, diabetes, others).
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Selected References
- Williams JS, Williams GH. Fifty years of aldosterone. J Clin Endo Metab, 2003; 88:2364-2372.
- Williams JS, Williams GH, Jeunemaitre X, Hopkins PN, Conlin PR. Influence of dietary sodium on the renin-angiotensin-aldosterone system and prevalence of left ventricular hypertrophy by EKG criteria. J H Hyperten 2005; 19:133-138.
- Williams JS, Solomon SD, Crivaro M, Conlin PR. Dietary sodium intake modulates myocardial relaxation responsiveness to angiotensin II. J Lab Clin Med (In Press).
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Contact Information:
(617) 278-0882
jwilliams5@partners.org |
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Send Feedback to: Jessica Hyde at jhyde@partners.org
This page was last modified on 2/10/2008
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