作者: Feng J. He , Nirmala D. Markandu , Giuseppe A. Sagnella , Hugh E. de Wardener , Graham A. MacGregor
DOI: 10.1161/01.HYP.0000149431.79450.A2
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摘要: Salt intake is a major regulator of blood pressure. There evidence that those who develop high pressure have an underlying defect in the ability kidney to excrete salt. It has been suggested this results greater tendency retain sodium and increased compensatory response responsible for rise also suggesting small increases plasma may directly affect pressure, independent associated expansion extracellular volume. We reanalyzed 3 types studies changing salt intake. (1) An acute large reduction from 350 mmol/d 10 20 5 days hypertensives normotensives was with fall approximately mmol/L (P<0.001). (2) Progressive 250 by daily amount 50 mmol caused (3) Longer-term modest studied double-blind randomized crossover studies; 1 month usual ( 170 mmol/d) compared reduced 100 mmol/d). decrease 0.4+/-0.2 (P<0.05), which weakly but significantly correlated systolic (r=0.18; P<0.05). These demonstrate increase or causes changes sodium. Small alter volume, influence Changes directly.