BACKGROUND: The study expands upon the findings of the DASH study, which showed that a dietary pattern emphasizing fruits, vegetables and low fat dairy products and is overall reduced in total and saturated fat significantly lowers blood pressure (BP). The DASH diet is particularly effective in African Americans and in individuals with systolic hypertension. However, it is not known if the DASH diet affects the pathophysiology of the hypertensive process. Preliminary data support the possibility that the DASH diet interrupts the renin-angiotensin system. This raises the intriguing possibility that the DASH diet will favorably impact on cardiovascular and renal hemodynamics in patients with isolated systolic hypertension. Therefore, the central hypothesis of this study is that the DASH diet affects central aortic stiffness, diastolic relaxation and renal and vascular reactivity to angiotensin II (Ang II) by lowering tissue renin-angiotensin system activity.

DESIGN NARRATIVE: A randomized, crossover design will be used to compare the DASH diet to a control diet as defined in the original DASH protocol (NEJM 1997; 336:1117). Fifty-five community-dwelling individuals age 20 and older with systolic blood pressure (SBP) 140-179 mmHg and diastolic blood pressure (DBP) < 90 mmHg will be randomized following a 2-week run-in on the control diet. Measurement will be taken just prior to randomization and at the conclusion of each 6-week interventional feeding period. Specific measurements will include: peripheral and renal vascular response to AII infusions, Renal Blood Flow by PAH, conduit vessel hemodynamics and tissue Doppler imaging (TDI). At the end of each interventional feeding period specific measurements will be made before and after captopril. Recruitment strategies will be identical to those successfully employed in the original DASH and DASH II studies. Measurements to verify BP, weight, urinary electrolyte excretion will be obtained.

The study will show that the DASH diet (1) lowers central aortic stiffness as measured by vascular impedance and carotid-femoral pulse wave velocity; (2) improves diastolic relaxation as measured by early diastolic myocardial velocities across the mitral valve (Ea); (3) vasodilates renal blood flow and enhances vascular responses to angiotensin II; and (4) affects central aortic stiffness, diastolic relaxation, renal blood flow, and renal and vascular reactivity to angiotensin II by altering target tissue responsiveness to angiotensin II similar to acetylcholinesterase (ACE) inhibition.