Author(s): Franco V, Oparil S
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Abstract High dietary sodium has been adduced as a cause of hypertension and its target organ damage for millennia; yet careful observations using sophisticated techniques have revealed only a weak relationship between sodium intake/excretion and blood pressure in the general population. Further, studies of the effects of dietary sodium reduction on blood pressure have revealed minimal achieved reductions in blood pressure, no relationship between the magnitude of reduction in sodium intake/excretion and the blood pressure effect, and no evidence of an effect of sodium reduction on death or cardiovascular events. While blood pressure in the population as a whole is only modestly responsive to alterations in sodium intake, some individuals manifest large blood pressure changes in response to acute or chronic salt depletion or repletion, and are termed "salt sensitive". Salt sensitivity and resistance have a large variety of determinants, including genetic factors, race/ethnicity, age, body mass and diet (overall diet quality, macro- and micronutrient content), as well as associated disease states, e.g. hypertension, diabetes and renal dysfunction. Salt sensitivity can be modulated by improving the quality of the diet, e.g. the DASH diet reduced salt sensitivity by increasing the slope of the pressure-natriuresis curve. Mechanisms that appear to contribute to salt sensitivity include blunted activity of the renin-angiotensin-aldosterone system, deficiency in atrial natriuretic peptide expression, and blunted arterial baroreflex sensitivity. Salt sensitivity in both normotensive and hypertensive persons has been associated with increased cardiovascular disease events and reduced survival. Increased attention to strategies that reduce salt sensitivity, i.e. improvement in diet quality and weight loss, particularly in high risk persons, is urgently needed.
This article was published in J Am Coll Nutr
and referenced in Journal of Pharmacogenomics & Pharmacoproteomics