The blood pressure of a significant percentage of the hypertensive population, and the normotensive population at a high risk for the development of hypertension (Blacks and older individuals), is sodium (salt)-dependent. That is to say, increasing the intake of salt will increase blood pressure in these individuals; conversely, and more importantly, decreasing the intake of salt will reduce blood pressure. The long-term objective of this research is to understand the mechanism(s) underlying sodium-dependent blood pressure control, and to determine the consequences thereof. We believe that the mechanisms are only indirectly linked to race, sex, and age. Our research is consistent with the hypothesis that sodium-dependent blood pressure control results from decreased responsiveness of the renal and adrenal blood pressure regulatory systems. This produces abnormal daily blood pressure patterns, with reduced fluctuation resulting in extended periods of increased blood pressure. The increased cardiovascular load leads to the early development of cardiovascular and renal disease, including hypertension. We will test this hypothesis by identifying "high risk" and "normal risk" subjects based on renal responses to sodium restriction. The subjects (n=200) will be equal numbers of healthy males and females, Blacks and Whites between the ages of 55-70 years. Using an innovative new approach, we will then examine the influence of risk status on 24-hour patterns of blood pressure, hormonal activity, and sodium handling. Finally, we will determine the clinical significance of the profiles by examining changes in cardiac and renal status at a two-year follow-up.
|Effective start/end date||1/1/93 → 12/31/96|
- National Institutes of Health
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