Role of dietary salt in hypertension.
Hypertension is the most common chronic disease in the United States and, untreated, results in disability or death due to stroke, heart failure or kidney failure. Fortunately the results of hypertension can be avoided to a large extent by proper treatment. One treatment which is effective in some cases is the restriction of dietary NaCl intake. This review considers the role of dietary NaCl in the genesis, therapy and prevention of hypertension. Most people can eat as much NaCl as they like; they have good kidneys which, within about 24 hours, excrete the NaCl as fast as it is taken in and nothing happens to blood pressure. A few, especially those with kidney disease, do not excrete it as fast as it is taken in and blood pressure rises. They are "salt sensitive". Once hypertension is established, the proportion who are "NaCl sensitive" is much higher. About 60% of people with hypertension respond to a high NaCl intake with a rise in pressure and to NaCl restriction with a fall in pressure and reduction in the need for antihypertensive medication. These are the same people that respond to diuretics with a fall in blood pressure. Many are black and elderly and have low plasma renin activity (low-renin hypertension) but some have normal or high plasma renin activity (normal or high-renin hypertension). Evidence suggests that very early they have a subtle kidney defect which causes them to excrete NaCl and water more slowly, e.g., even before they become hypertensive, black and elderly subjects excrete intravenously administered NaCl more slowly than white and young subjects. How does NaCl retention raise blood pressure? One possibility is that the NaCl retention causes water retention which releases a digitalis-like substance that increases the contractile activity of heart and blood vessels. Another is that the sodium itself penetrates the vascular smooth muscle cell, causing it to contract. "Salt sensitive" hypertension also responds to increased potassium and calcium intakes, perhaps in part because they increase NaCl urinary excretion.
Department of Physiology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814-4799, USA.
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Haddy
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Pamnani
D000367:Age Factors; D000368:Aged; D044383:Black People; D002136:Calcium, Dietary; D004039:Diet, Sodium-Restricted; D004195:Disease Models, Animal; D006801:Humans; D006973:Hypertension / Q000139:chemically induced* / Q000378:metabolism / Q000517:prevention & control; D017419:Potassium, Dietary; D012307:Risk Factors; D017673:Sodium Chloride, Dietary / Q000009:adverse effects* / Q000378:metabolism
D002136:Calcium, Dietary; D017419:Potassium, Dietary; D017673:Sodium Chloride, Dietary