Abstract
See related article, pp 180–185 Blood pressure is responsive to sodium intake in many patients with essential hypertension. It seems that subjects of African-American ancestry and older subjects are most sensitive to salt.1 Yet, there is no agreement on how such salt sensitivity is determined: frequently, such measurements involve 2 different periods on high- and low-sodium diets; others involve intravenous sodium loading and then low-salt diet and furosemide depletion. In different studies, the definition of salt sensitivity and related procedures differ substantially and quite arbitrarily (or perhaps empirically).1,–,3 Regardless of definition, in research settings salt loading or depletion is short term, while in reality, it is the long-term exposure that counts, especially with the recent recognition that sodium can accumulate in the skin and perhaps other tissues.4 Hypertensive subjects with salt sensitivity retain salt. However, salt retention also exists in other conditions. In renal failure, it is likely to be associated with hypertension, while not necessarily so in heart failure or cirrhosis of the liver. Healthy subjects with normal blood pressure may also be salt sensitive and are then more likely to become hypertensive over time.1 In individuals with salt-sensitive hypertension, high sodium intake expands vascular volume, and arterial pressure rises along with cardiac output. Urinary sodium excretion increases in parallel to blood pressure elevation, but balance is maintained at increased vascular pressures compared …
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