Hypertension, Vol 7, 628-640, Copyright © 1985 by American Heart Association
GA MacGregor
There is much circumstantial and some direct evidence in humans to suggest
that a high consumption of salt predisposes communities and individuals to
the development of essential hypertension. Recent work has suggested
possible mechanisms whereby a high salt intake could cause a rise in blood
pressure in genetically susceptible persons. Restriction of salt intake in
the diet lowers blood pressure in many subjects with high blood pressure
and this fall in blood pressure is mediated in part by a diminished renin
response to sodium restriction as hypertension develops. The effect of
sodium restriction, like diuretics, is additive to most blood pressure
lowering drugs, particularly those that inhibit the renin system such as
beta-blockers and angiotensin converting enzyme inhibitors. Claims that a
slight reduction in calcium intake may be important in the development of
high blood pressure are disputed. Furthermore, no satisfactory hypothesis
has been put forward to explain how a small reduction in dietary calcium
intake could cause high blood pressure. Large increases in calcium intake
have been reported to lower blood pressure in both normotensive and
hypertensive humans. The three published studies, however, are not in
agreement.
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Sodium is more important than calcium in essential hypertension
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