8211 Saturday 10 January 1981 BLOOD PRESSURE AND HORMONAL CHANGES FOLLOWING ALTERATION IN DIETARY SODIUM AND POTASSIUM IN MILD ESSENTIAL HYPERTENSION P. S. PARFREY P. WRIGHT F. J. GOODWIN M. J. VANDENBURG J. M. P. HOLLY S. J. W. EVANS J. M. LEDINGHAM Medical and Steroid Units, London Hospital Medical College, London E1 Summary Sixteen patients with mild essential hypertension (average diastolic blood pressure 90-110 mm Hg) and eight normotensive subjects (diastolic pressure less than 85 mm Hg) were studied in a ran- domly allocated, crossover, observer-blind trial in which they received their normal diets supplemented by 100 mmol sodium daily for 12 weeks and a no added sodium diet sup- plemented by 100 mmol potassium daily for the same period. During the high sodium diet blood pressure (BP) rose slowly in both groups. At 12 weeks systolic pressure was significant- ly (8·9±12·6, mean ±SD mm Hg) higher than pre-diet levels in the hypertensive group and 5· 3±9· 0 mm Hg higher in the normotensive group (not significant). During the high potassium/no added sodium diet, BP fell sharply in the hypertensive group. At 6 weeks the mean systolic pressure was 8· 9±11· 2 mm Hg lower than pre-diet levels whereas in the normotensive group it was 3· 7 higher, the difference in response being significant. There were no significant dif- ferences in plasma renin and aldosterone between the two groups at the start of the trial, whereas plasma noradrenaline, measured in the supine resting state, was significantly higher in the hypertensive group. During the high sodium phase, the levels of all three hormones fell, but only the fall in plasma noradrenaline in the hypertensive group was significant. During the high potassium/low sodium phase, there was little change in plasma renin and noradrenaline, whereas plasma aldosterone rose significantly in both groups. Correlations were observed between changes in BP and in the urinary Na/K ratio in the hypertensive group during the trial, but no consistent correlations were found between changes in BP and in hormonal levels. The BP of patients with mild essen- tial hypertension, but not of normotensive subjects, is lowered by moderately reducing dietary sodium and increas- ing potasssium. The mechanism of this action is unlikely ex- clusively to involve changes in plasma renin, aldosterone, or noradrenaline. Introduction REDUCTION of dietary sodium has been advocated for the management of hypertension for many years,I,2 but its ef- ficacy depended on a regimen which was too restrictive for long term application.3,4 Recently, more modest restrictions of sodium intake over periods of one month5 and two years6 were reported to lower blood pressure significantly. Although potassium administration ameliorates salt hypertension occurring in stock7,S and salt-sensitive’," rats and reduces the blood pressure of Okamoto spontaneously hypertensive rats," few studies of chronic administration to hypertensive man have been done. 12-14 The possibility that patients with essential hypertension may be specifically sen- sitive to changes in sodium and potassium intake does not ap- pear to have been investigated. We set out to explore this possibility by modifying, in the long term, the dietary intake of sodium and potassium in patients with essential hyperten- sion and in normotensive subjects and to follow the blood pressure (BP) and plasma levels of certain hormones involved in BP regulation. Patients, Controls, and Methods Subjects Sixteen hypertensive patients aged 26-49 years and eight normal subjects aged 26-39 years were studied. The patients were newly diagnosed and untreated and were shown to have essential hyperten- sion by exclusion of known primary causes. They were accepted for the trial if their average lying diastolic pressure, measured on four occasions at least a week apart, lay between 90 and 110 mm Hg. The eight normal subjects were hospital personnel with no family history of hypertension and whose average diastolic pressure, taken on four occasions, was less than 85 mm Hg. Design The subjects attended a special research clinic at a fixed hour and day of the week on each visit. On arrival BP was taken twice after 5 min resting supine and then twice after standing for 5 min, phases I and V being recorded by a bias-free technique with the London School of Hygiene sphygmomanometer. Heart rate was measured over 30 s from the radial pulse in both positions. Blood was taken for the measurement of plasma renin and aldosterone (ambulatory samples) after which an indwelling needle was left in the antecubital vein while the patient rested supine for an hour. BP was then measured twice and blood was taken for plasma renin, aldosterone, and noradrenaline (supine samples). After standing for 5 min BP was measured twice more and a further blood sample taken for estimation of plasma noradrenaline (standing sample). After four screening visits, patients and normal subjects were ad- mitted to the trial and randomly allocated to either a high potassium,