Salt Sensitivity and Hypertension in African Americans: Implications for Cardiovascular Disease

Rosalind M. Peters, MSN, RN, John M. Flack, MD, MPH


Prog Cardiovasc Nurs. 2000;15(4) 

In This Article

Salt Sensitivity Conceptualized and Defined

Worldwide epidemiologic studies have demonstrated that habitual ingestion of high levels of dietary salt (NaCl) is associated with increased blood pressure.[6,7] In populations whose dietary salt intake is <100 mmol/day, hypertension is rare, and the trend of rising blood pressure with advancing age, particularly systolic blood pressure (SBP), does not occur. As the aggregate level of salt ingestion increases, so does the prevalence of hypertension.[8,9] The average American consumes more than 150 mmol -- or almost 4 gm -- of sodium each day, which may be a significant factor in the rates of hypertension found in the U.S. However, ecologic studies provide insufficient evidence to establish a causal link between sodium ingestion and hypertension. In addition, they do not explain the significant heterogeneity among individuals in blood pressure sensitivity to sodium intake. For these reasons, a number of experimental studies have been conducted to examine the phenomenon of salt sensitivity and its relationship to blood pressure.

Conceptually, salt sensitivity is defined as an increase in blood pressure in response to increased sodium ingestion and/or a decrease in blood pressure when sodium intake is reduced, with the degree of change exceeding that attributed to directionally appropriate random blood pressure variation. Salt sensitivity results from alterations in kidney function that require higher arterial pressure to maintain "steady-state" homeostasis, and is reflected in a "resetting," or a shifting to the right, of the pressure-natriuresis curve.[10,11,12] That is, a higher blood pressure level is required to excrete a given amount of dietary sodium.

Operational definitions of salt sensitivity have been arbitrary and varied. They may reflect changes in systolic, diastolic, or mean arterial blood pressure (MAP), which is calculated as (2X (DBP) + SBP/3].[7,8,9] Usually, the change in diastolic or MAP is used to define salt sensitivity. However, on a per mm Hg basis, salt has a greater impact on systolic pressure than on either diastolic or mean arterial pressure. Some researchers define salt sensitivity as a fixed, arbitrary change in pressure (i.e., more than a 3 mm Hg directionally appropriate change), while others define it as a directionally appropriate proportional change (i.e., a 10% change in pressure).[12] Some studies have used a single, arbitrary, unidirectional blood pressure change as evidence of salt sensitivity. However, these findings must be interpreted cautiously, as these designs may not reliably disentangle salt sensitivity from normal random variability of blood pressure because blood pressure randomly fluctuates upward and downward in all persons, within a fairly predictable range.[8,10] In addition to a variation in definitions, a variety of protocols have been used to determine salt sensitivity. Some studies used rapid i.v. salt loading followed by furosemide-induced volume depletion to determine the influence of salt on blood, while other studies manipulated the amount of dietary sodium ingested by research subjects to test for salt sensitivity.[13,14,15,16] The relationship of blood pressure changes after rapid i.v. saline loading or diuretic-induced volume depletion to blood pressure changes after dietary manipulation of salt intake is unknown. However, regardless of the variability noted in both the design and definition of salt sensitivity, there are several factors that have consistently emerged as being associated with salt sensitivity across all studies.


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