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(Hypertension. 2001;38:321.)
© 2001 American Heart Association, Inc.
Scientific Contributions |
Blood Pressure Unit, St. Georges Hospital Medical School, London, United Kingdom.
Correspondence to Prof G.A. MacGregor, Blood Pressure Unit, St. Georges Hospital Medical School, Cranmer Terrace, London, SW17 0RE, UK. E-mail g.macgregor{at}sghms.ac.uk
Abstract Hypertensive (n=93) and normotensive (n=39) white individuals were given a high sodium intake of
350 mmol/d for 5 days followed by a low sodium intake of 10 to 20 mmol/d for 5 days. With this acute and large reduction in salt intake, no significant change was seen in blood pressure in the normotensive individuals, but blood pressure decreased in the hypertensive individuals. Compared with normotensive subjects, hypertensive patients had a 7/7-mm Hg greater fall in blood pressure (P<0.05 for systolic and P<0.01 for diastolic, adjusted for age), with similar changes in urinary sodium excretion. From the high-salt to low-salt diet, plasma renin activity rose from 0.90 to 5.99 ng · mL-1 · h-1 in normotensives, whereas in hypertensives it rose from 0.73 to only 3.14 ng · mL-1 · h-1 (P<0.05 between hypertensives and normotensives). Plasma aldosterone rose by 1396 pmol/L in normotensive subjects and by 511 pmol/L in hypertensive patients (P<0.05). Significant inverse correlations were obtained for all subjects between the fall in blood pressure from the high-salt to low-salt diet and the rise in plasma renin activity and aldosterone that occurred in addition to the absolute level on the low-salt diet. These results demonstrate that the larger fall in blood pressure with an acute reduction in salt intake in hypertensives compared with normotensives is, at least in part, due to a less-responsive renin-angiotensin-aldosterone system in the hypertensive patients.
Key Words: renin-angiotensin system blood pressure sodium diet, sodium-restricted hypertension, essential normotension
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