Dietary sodium and arterial blood pressure: evidence against genetic susceptibility. Salt restriction: effects on lipids and insulin production in hypertensive patients. Effect of dietary sodium intake on blood lipids: results from the DASH-sodium trial. A low-sodium diet supplemented with fish oil lowers blood pressure in the elderly. Moderate sodium restriction and diuretics in the treatment of hypertension. Enhanced blood pressure response to dietary salt in elderly women, especially those with small waist: hip ratio. The effects of nonpharmacologic interventions on blood pressure of persons with high normal levels. Results of the Trials of Hypertension Prevention, Phase I. Effect of sodium chloride- and sodium bicarbonate-rich mineral water on blood pressure and metabolic parameters in elderly normotensive individuals: a randomized double-blind crossover trial. Beta blockade, diuretics, and salt restriction for the management of mild hypertension: a randomised double blind trial. Double-blind randomised crossover trial of moderate sodium restriction in essential hypertension. Double-blind randomised trial of modest salt restriction in older people. Moderate salt restriction effectively lowers blood pressure and degree of salt sensitivity is related to baseline concentration of renin and N-terminal atrial natriuretic peptide in plasma. Evaluation of the effectiveness of a low sodium diet in the treatment of mild to moderate hypertension. Double-blind study of three sodium intakes and long-term effects of sodium restriction in essential hypertension. Sodium restriction and potassium supplementation in young people with mildly elevated blood pressure. Blood-pressure response to moderate sodium restriction and to potassium supplementation in mild essential hypertension. Effect of modest salt reduction on blood pressure, urinary albumin, and pulse wave velocity in white, black, and Asian mild hypertensives. Modest salt reduction reduces blood pressure and urine protein excretion in black hypertensives: a randomized control trial. Arterial effects of salt restriction in hypertensive patients. A 9-week, randomized, double-blind, crossover study. Dietary sodium restriction rapidly improves large elastic artery compliance in older adults with systolic hypertension. Effects of moderate sodium restriction on clinic and twenty-four-hour ambulatory blood pressure in elderly hypertensive subjects. Neurohormonal and metabolic effects of severe and moderate salt restriction in non-obese normotensive adults.
Thirty five subjects with both parents in the top third of their age specific blood pressure distributions and 31 subjects with both parents in the bottom third of their blood pressure distributions restricted their intake of sodium for eight weeks while taking part in a double blind, randomised crossover trial of supplements of sodium and placebo. A comparison of two periods of four weeks at different intakes of sodium showed no differences in blood pressure in either the groups as a whole or the subgroups who complied best with the diet and tablets. In the compliant subgroups mean urinary sodium excretions were above 120 mmol(mEq) and below 50 mmol/day. The study provides evidence against the hypothesis that people with a family history of high blood pressure are more susceptible in their blood pressure response to dietary sodium. The object of the study was to evaluate blood pressure, insulin and glucose metabolism, and serum lipids in hypertensive patients, during 8 weeks on a moderately salt-restricted diet. A double-blind, cross-over study was conducted with hypertensive patients following a moderately salt-restricted diet. Patients were randomised to sodium capsules in one period and placebo capsules during the other period. After a 1-month run-in period, 13 males and three females with mild to moderate essential hypertension (mean age 50 years) complied with a salt-reduced diet. They were randomized to a salt-supplemented group (5 capsules of 10 mmol sodium per capsule) or a salt reduced diet group (5 capsules of placebo) with cross-over after 8 weeks. Serum insulin, insulin C-peptide, and glucose were measured, fasting and 30 min after a 75-g glucose load. Serum lipids and lipoproteins constituting an atherogenic index were measured, along with blood pressure and 24-h urine excretion of sodium and chloride. Non-significant reductions of systolic and diastolic blood pressure (4 mmHg, p = 0.06, and 2 mmHg, p = 0.13, respectively) were observed during the reduced-salt period. The changes observed for fasting insulin, insulin C-peptide, glucose, serum lipids and the atherogenic index were also non-significant. It is concluded that moderate salt restriction seems not to adversely influence insulin resistance or serum lipids in hypertensive patients. We evaluated the effect on serum lipids of sodium intake in 2 diets. Participants were randomly assigned to a typical American control diet or the Dietary Approaches to Stop Hypertension (DASH) diet, each prepared with 3 levels of sodium (targeted at 50, 100, and 150 mmol/d per 2100 kcal). The DASH diet is increased in fruits, vegetables, and low-fat dairy products and is reduced in saturated and total fat. Within assigned diet, participants ate each sodium level for 30 days. The order of sodium intake was random. Participants were 390 adults, age 22 years or older, with blood pressure of 120 to 159 mm Hg systolic and 80 to 95 mm Hg diastolic. Serum lipids were measured at baseline and at the end of each sodium period. Within each diet, sodium intake did not significantly affect serum total cholesterol, LDL cholesterol, HDL cholesterol, or triglycerides. On the control diet, the ratio of total cholesterol-to-HDL cholesterol increased by 2% from 4.53 on higher sodium to 4.63 on lower sodium intake (P=0.04). On the DASH diet, sodium intake did not affect this ratio. There was no dose-response of sodium intake on serum lipids or the cholesterol ratio in either diet. At each sodium level, total cholesterol, LDL cholesterol, and HDL cholesterol were lower on the DASH diet versus the typical American diet. There were no significant interactions between the effects of sodium and the DASH diet on serum lipids. In conclusion, changes in dietary sodium intake over the range of 50 to 150 mmol/d did not affect blood lipid concentrations. To examine effects of dietary fish oil supplementation with sodium restriction on blood pressure in the elderly.
                In a double-blind dietary intervention lasting 4 weeks, parallel comparisons of blood pressure were made in volunteers assigned to one of four treatment groups: fish oil and low sodium; fish oil and normal sodium; sunflower oil and low sodium; or sunflower oil and normal sodium.
                Subjects lived at home and attended our nutrition research clinic at fortnightly intervals for dietary counselling and blood pressure measurement.
                Health volunteers aged 60-80 years were sought by advertisement. A total of 114 men and women were enrolled in two cohorts; 106, with an initial mean blood pressure of 132/77 mmHg, satisfactorily completed the study.
                All subjects adopted a low-sodium diet and dietary changes were effected by double-blind administration of slow-release sodium chloride or placebo tablets, along with capsules containing either fish or sunflower oil.
                The primary measure was the within-subject change in blood pressure after 4 weeks of intervention in each dietary treatment group.
                Urinary sodium excretion in subjects on low-sodium diets decreased whilst potassium excretion was unaffected. Systolic blood pressure (SBP) fell in the group taking sunflower oil with low sodium, but there was only a transient fall in diastolic blood pressure (DBP). In those taking fish oil with normal sodium, the change in blood pressure was not significant, except after adjustment for initial blood pressure and weight changes. When fish oil was combined with low sodium, however, both SBP and DBP were substantially reduced; the reduction in DBP was significantly greater than in the other treatment groups.
                Dietary fish oil and sodium restriction can interact to lower DBP in the elderly. nan To determine the blood pressure responses in elderly normotensive men and women to dietary sodium and to the diunsaturated fatty acid dihomogammalinolenic acid (DGLA), which is derived from linoleic acid.
                Blood pressure responses were assessed in 66 subjects (36 male, 30 female; mean age 65 years) on two diets differing by approximately 70 mmol/day sodium, combined with daily supplements of either 1 g DGLA or 1 g safflower oil, giving a four-group parallel design. After a common period of salt restriction and salt supplementation, two sets of parallel groups continued with either salt or placebo tablets. The study was blinded, except for dietary adjustments based on 24-h urinary sodium excretion values measured once every 2 weeks. Blood pressures were also measured automatically once every 2 weeks.
                Urinary sodium excretion (sodium intake) correlated significantly with systolic and diastolic blood pressures. A strong interaction with sex (P < 0.001 for systolic blood pressure) reflected greater responsiveness in women to changing sodium intake. A second major determinant of blood pressure responsiveness was the waist: hip ratio, an index of central obesity; this correlation was independent of the initial sodium intake, initial blood pressure or body mass index. The waist: hip ratio was a powerful predictor of blood pressure changes with sodium intake in women only; women with android fat distribution were, similarly to men, less sensitive to dietary sodium. Daily supplements of 1 g DGLA doubled the concentration of DGLA in plasma but did not influence blood pressure.
                Among elderly normotensive subjects, women responded to changes in sodium intake with greater changes in blood pressure than men did. Furthermore, this response was strongly related to the gynaecoid distribution of body fat. To test the short-term feasibility and efficacy of seven nonpharmacologic interventions in persons with high normal diastolic blood pressure.
                Randomized control multicenter trials.
                Volunteers recruited from the community, treated and followed up at special clinics.
                Of 16,821 screenees, 2182 men and women, aged 30 through 54 years, with diastolic blood pressure from 80 through 89 mm Hg were selected. Of these, 50 did not return for follow-up blood pressure measurements.
                Three life-style change groups (weight reduction, sodium reduction, and stress management) were each compared with unmasked nonintervention controls over 18 months. Four nutritional supplement groups (calcium, magnesium, potassium, and fish oil) were each compared singly, in double-blind fashion, with placebo controls over 6 months.
                Primary: change in diastolic blood pressure from baseline to final follow-up, measured by blinded observers. Secondary: changes in systolic blood pressure and intervention compliance measures.
                Weight reduction intervention produced weight loss of 3.9 kg (P less than .01), diastolic blood pressure change of -2.3 mm Hg (P less than .01), and systolic blood pressure change of -2.9 mm Hg (P less than .01). Sodium reduction interventions lowered urinary sodium excretion by 44 mmol/24 h (P less than .01), diastolic blood pressure by 0.9 mm Hg (P less than .05), and systolic blood pressure by 1.7 mm Hg (P less than .01). Despite good compliance, neither stress management nor nutritional supplements reduced diastolic blood pressure or systolic blood pressure significantly (P greater than .05).
                Weight reduction is the most effective of the strategies tested for reducing blood pressure in normotensive persons. Sodium reduction is also effective. The long-term effects of weight reduction and sodium reduction, alone and in combination, require further evaluation. To examine the effect of sodium chloride- and sodium bicarbonate-rich mineral water on blood pressure and parameters of glucose and lipid metabolism in elderly normotensive individuals.
                We examined 21 healthy men and women aged 60-72 years in a randomized, placebo-controlled, double-blind crossover trial. After reducing dietary salt intake to below 100 mmol/day, study participants were randomly assigned to drink 1.5 l daily of a sodium chloride-rich (sodium 84.5 mmol/l, chloride 63.7 mmol/l, bicarbonate 21.9 mmol/l), a sodium bicarbonate-rich (sodium 39.3 mmol/l, chloride 6.5 mmol/l, bicarbonate 48.8 mmol/l) and a low-sodium (placebo: sodium, chloride and bicarbonate < 0.02 mmol/l) mineral water for 4 weeks each in a three-phase crossover order. Each phase was separated by a 2-week washout period in which the study participants remained on a low-salt diet. Compliance was assessed by biweekly urinary electrolyte excretion and five study participants were excluded from analysis for failing to complete the trial or to fulfil the compliance criteria.
                Mean arterial blood pressure was significantly lower during the periods of consuming low-sodium -7.0 +/- 7.2 mmHg, P < 0.001) or sodium bicarbonate-rich (-5.7 +/- 6.4 mmHg, P < 0.05) water than at baseline. In contrast, blood pressure during the phase of drinking sodium chloride-rich water was identical to that at baseline. Ambulatory 24 h blood pressure, oral glucose tolerance and plasma lipids were not affected by the different regimens. Urinary calcium excretion was significantly reduced by drinking low-sodium or sodium bicarbonate-rich water but was unchanged under the sodium chloride-rich water.
                Consumption of sodium chloride-rich mineral water can abolish the blood pressure reduction induced by dietary salt restriction in elderly individuals. Sodium bicarbonate-rich mineral water in conjunction with a low-salt diet may have a beneficial effect on calcium homeostasis. Ninety four patients with mild hypertension (average supine diastolic blood pressure (phase V) 95-110 mm Hg) were allocated at random to receive restriction of dietary sodium (maximum allowed 70 mmol(mEq)/24 h) or a normal diet. In addition, they received in random order 25 mg chlorthalidone, 200 mg metoprolol (slow release), and a fixed combination of these two drugs. Each drug treatment was given for four weeks and alternated with four weeks of placebo. Forty four patients were allocated to sodium restriction (group 1) and 50 to normal diet (group 2). The mean 24 hour urinary sodium excretion in group 1 was 74 (SD 31) mmol(mEq)/24 h, and in group 2 132 (51) mmol/24 h. Compared with the screening blood pressure the average decrement of the supine blood pressure in group 1 was 16.0/8.6 mm Hg with placebo, 21.7/11.5 mm Hg with the diuretic, 28.5/17.8 mm Hg with the beta blocker, and 28.9/18.4 mm Hg with the combined agent; in group 2 these values were 13.3/6.1, 20.3/9.7, 21.3/12.9, and 29.4/16.8 mm Hg, respectively. There was a sharp decrease of the average potassium concentration during chlorthalidone and combination treatment periods (average value 3.3 mmol(mEq)/1). These results suggest that moderate salt restriction used as sole treatment has a limited though demonstrable blood pressure lowering effect but that when it is used as an adjuvant to beta blocker treatment its value is greatly enhanced. Nineteen unselected patients with mild to moderate essential hypertension, whose average supine blood pressure after two months' observation on no treatment was 156/98 mm Hg, were advised not to add salt to food and to avoid sodium-laden foods. After 2 weeks of sodium restriction patients were entered into an 8-week double-blind randomised crossover study of 'Slow Sodium' (Ciba) versus slow sodium placebo. The mean supine blood pressure was 7.1 mm Hg (6.1%) lower in the fourth week of placebo than that in the fourth week of slow sodium (p less than 0.001). Urinary sodium excretion in the fourth week of slow sodium was 162 +/- 9 mmol/24 h and that in the fourth week of placebo was 86 mmol +/- 9 mmol/24 h (p less than 0.001). There was no difference in potassium excretion. These results suggest that moderate sodium restriction achieved by not adding salt and avoiding sodium-laden foods should, if not already, become part of the management of essential hypertension. Stroke is directly related to blood pressure and treatment trials in older hypertensive individuals show a reduction in strokes. However, the majority of strokes occur in normotensive individuals in whom no attempt is made to lower blood pressure. We compared the effects of modest salt restriction on blood pressure in older hypertensive and normotensive people.
                47 untreated elderly people (24 men, age range 60-78 years; blood-pressure range 123-205 mm Hg systolic and 64-112 mm Hg diastolic) completed a 2-month double-blind randomised placebo-controlled crossover study of modest salt restriction with slow sodium and placebo to give a salt intake of either 10 g (equivalent to the normal amount for the UK population) or 5 g.
                On the normal salt intake for the UK population, supine blood pressure was 163/90 (SD 21/10) mm Hg with urinary sodium excretion of 177 (49) mmol/day. With modest sodium restriction, blood pressure fell to 156/87 (22/9) mm Hg (p < 0.001/0.004) with a urinary sodium excretion of 94 (50) mmol/day. A reduction in sodium intake of 83 mmol/day was associated with a reduction of 7.2/3.2 mm Hg. There was no significant difference in the blood-pressure fall between 18 normotensive and 29 hypertensive participants (8.2/3.9 vs 6.6/2.7 mm Hg).
                A modest reduction in salt intake leads to a fall in blood pressure in both normotensive and hypertensive older people similar to that in outcome trials of thiazide-based treatment. Since the majority of strokes in older people occur below the current definition of hypertension, our results have important implications for the prevention of stroke. The effect of salt restriction on blood pressure is under intense debate. We tested the effect of 100 mmol salt reduction on ambulatory blood pressure (ABP) in 46 Swedish individuals, 39 of whom completed the study, using a double-blind, placebo-controlled, cross-over design. Furthermore, we tested whether the basal plasma concentration of renin or N-terminal atrial natriuretic peptide (Nt-proANP) predict the degree of salt sensitivity.
                Participants received all meals and drinks with a total daily NaCl content of 50 mmol during 8 weeks. In addition, NaCl capsules (100 mmol/day) and corresponding placebo capsules were administered for 4 weeks each in random order. ABP after high-salt intake (150 mmol/day) was compared with ABP after low-salt intake (50 mmol/day). Salt sensitivity was defined as the difference between 24-h systolic ABP at the high-salt versus the low-salt periods. Baseline renin and Nt-proANP were related to salt sensitivity.
                Lowering of salt intake from 150 to 50 mmol/day induced significant blood pressure reductions (mean reduction, 95% confidence interval) in systolic and diastolic 24-h ABP (5.8, 3.4-8.2 and 2.6, 0.91-4.4 mmHg), daytime ABP (5.5, 2.9-8.1 and 2.3, 0.42-4.1 mmHg) and night-time ABP (6.4, 3.5-9.3 and 3.4, 1.4-5.5 mmHg). Baseline ln(renin) correlated inversely with salt sensitivity (r = -0.50, P = 0.001) whereas baseline ln(Nt-proANP) correlated directly (r = 0.33, P = 0.04).
                Lowering of salt intake with 100 mmol/day induces clinically relevant ABP reductions. Renin and Nt-proANP, measured with individuals on their habitual diet, could be useful biomarkers to identify individuals with the greatest blood pressure-lowering benefit from reduced salt intake. 28 patients who had a sustained diastolic blood pressure of 95 to 104 mm Hg and who had no treatment for it for at least 13 months before the trial, but who were otherwise unselected, took part in a randomised controlled trial in which the effect of a restricted sodium diet was compared with that of a general health package. The general health package did not include any specific hypotensive procedures. Changes in blood pressure were measured at predetermined intervals over the course of a year. Within each group both systolic and diastolic blood pressure fell to a highly significant extent after a year, but there was no significant difference between the groups. It would thus seem that the antihypertensive effect of a restricted sodium diet may be related to the increased consultation and monitoring activity of such intervention rather than to the dietary manipulation itself. 20 patients with mild hypertension (average supine blood pressure without treatment, 164/101 mm Hg) reduced their salt intake to 50 mmol (3 g) per day for a month. They then entered a 3 month double-blind randomised crossover study of three levels of sodium intake: 200, 100, and 50 mmol per day. Blood pressure was significantly reduced on the middle and lowest sodium intakes. The average fall in blood pressure from the highest to the lowest sodium intake was 16/9 mm Hg. Patients continued to restrict their sodium intake for a further year. In 16 of the 20 patients blood pressure remained well controlled with salt restriction alone. Supine blood pressure at 1 year was 142/87 (SE 3/2) mm Hg with a 24 h urinary sodium excretion of 54 (7) mmol. These results show a progressive blood pressure fall as salt intake is reduced and that, in many patients with mild essential hypertension, blood pressure can be controlled without the need for drug therapy. Forty young subjects, aged 18 to 28 years, with mildly elevated blood pressure participated in a double-blind randomized three-period crossover study of the effect of sodium restriction with and without potassium supplementation on blood pressure. Dietary sodium intake was restricted for 18 weeks in which the patients received in random sequence 'slow-sodium' (90 mmol/day), 'slow-potassium' (72 mmol/day), and placebo tablets, each for 6 weeks. Mean urinary sodium excretion was 129 mmol/24 h in the slow-sodium period, 57 mmol/24 h during placebo, and 69 mmol/24 h during slow-potassium. Mean supine systolic blood pressure in the sixth week of the slow-potassium period was 3.3 mmHg lower than that at the end of the slow-sodium period (P less than 0.05). There was no significant difference in systolic or diastolic blood pressure between the placebo and the slow-sodium periods. The fall in systolic blood pressure in the low sodium/high potassium period was accompanied by a fall in cardiac index of 0.4 l/min per m2 body surface area (BSA) (P = 0.03). Our observations suggest a small hypotensive effect of moderate sodium restriction combined with high potassium intake in young hypertensive subjects. Sodium restriction alone has little effect on blood pressure in this group. The combination of a low sodium/high potassium diet may lower blood pressure by affecting cardiac output. Reducing the dietary sodium:potassium ratio may therefore be useful in the management of early primary hypertension. To determine whether moderate restriction of dietary sodium content or supplementation of potassium intake reduces blood-pressure in patients with mild essential hypertension, twelve patients were put on three different diets--a control diet (180 mmol sodium/day), a sodium restricted diet (80 mmol/day). Each diet was taken for at least 4 weeks and the sequence of the regimens was randomised. At the completion of each regimen intra-arterial pressure was recorded continuously, and vasoactive hormones were measured hourly, for 24 h, under standardised conditions, in hospital. Compared with the control diet, sodium restriction was associated with lower blood-pressure readings in seven patients, higher levels in five, and an overall reduction in mean pressures of only 4.0/3.0 mm Hg (not significant). Individual differences in blood-pressure between these two diets correlated closely with concomitant differences in plasma renin activity (r = 0.75). Potassium supplementation also resulted in variable changes in arterial pressure, and the mean difference in pressure recordings (0.1/0.8 mm Hg) was insignificant. The results show that moderate restriction of sodium intake or supplementation of dietary potassium has variable effects on arterial pressure in individuals with mild essential hypertension, and that overall the blood-pressure changes induced are very small. Responsiveness of the renin-angiotensin system may limit the fall in blood-pressure induced by sodium restriction. A reduction in salt intake lowers blood pressure. However, most previous trials were in whites with few in blacks and Asians. Salt reduction may also reduce other cardiovascular risk factors (eg, urinary albumin excretion, arterial stiffness). However, few well-controlled trials have studied these effects. We carried out a randomized double-blind crossover trial of salt restriction with slow sodium or placebo, each for 6 weeks, in 71 whites, 69 blacks, and 29 Asians with untreated mildly raised blood pressure. From slow sodium to placebo, urinary sodium was reduced from 165+/-58 (+/-SD) to 110+/-49 mmol/24 hours (9.7 to 6.5 g/d salt). With this reduction in salt intake, there was a significant decrease in blood pressure from 146+/-13/91+/-8 to 141+/-12/88+/-9 mm Hg (P<0.001), urinary albumin from 10.2 (IQR: 6.8 to 18.9) to 9.1 (6.6 to 14.0) mg/24 hours (P<0.001), albumin/creatinine ratio from 0.81 (0.47 to 1.43) to 0.66 (0.44 to 1.22) mg/mmol (P<0.001), and carotid-femoral pulse wave velocity from 11.5+/-2.3 to 11.1+/-1.9 m/s (P<0.01). Subgroup analysis showed that the reductions in blood pressure and urinary albumin/creatinine ratio were significant in all groups, and the decrease in pulse wave velocity was significant in blacks only. These results demonstrate that a modest reduction in salt intake, approximately the amount of the current public health recommendations, causes significant falls in blood pressure in all 3 ethnic groups. Furthermore, it reduces urinary albumin and improves large artery compliance. Although both could be attributable to the falls in blood pressure, they may carry additional benefits on reducing cardiovascular disease above that obtained from the blood pressure falls alone. High blood pressure and proteinuria are the major risk factors for cardiovascular and renal disease. In black individuals, there is an increased risk of hypertension, stroke, heart failure, and kidney disease. There are no controlled studies of the effects of reducing salt intake on blood pressure and urine protein excretion in black individuals. Therefore, the aim of our study was to determine the effects of modest salt restriction on blood pressure and urine protein excretion in nondiabetic black hypertensive subjects. The study was randomized, double blind, and placebo controlled. After run-in periods on their usual diet and on reduced salt, participants continued to restrict their salt intake and then received either slow sodium tablets, designed to bring their salt intake back to normal, or placebo tablets for 4 weeks in a randomized, double-blind, crossover study. In the 40 who completed the study, urinary sodium excretion fell on slow sodium to placebo from 169+/-73 to 89+/-52 mmol per 24 hours (P<0.001; approximately 10 to 5 g salt per day). Blood pressure fell from 159/101+/-13/8 to 151/98+/-13/8 mm Hg (P<0.01). Protein excretion fell from 93+/-48 mg to 75+/-30 mg per 24 hours (P<0.008). Thus, reducing salt intake from approximately 10 to 5 g per day reduced blood pressure and urine protein excretion in black hypertensives. In light of these findings, we would recommend that all black individuals with raised blood pressure reduce their salt intake to < or =5 g per day. To investigate the hemodynamic effects of a moderately low-salt diet in a 9-week, randomized, double-blind, crossover study in 20 hypertensive, ambulatory patients.
                All subjects followed a 9-week, low-salt diet. During this period, they received capsules containing either lactose or salt in 4-week treatment periods, separated by a 1-week washout period. Hemodynamic and biological parameters were evaluated on the day of randomization and at the end of weeks 4 and 9. We defined a low-sodium diet (LSD) as a salt-restriction period with lactose capsules, and a normal-sodium diet (NSD) as a salt-restriction period with capsular salt supplementation.
                Blood pressure was significantly lower during LSD compared with NSD. This fall in blood pressure was associated with a decrease in peripheral resistance in carotid and forearm circulation. Brachial artery diameter was larger during LSD whereas carotid artery diameter remained unchanged. The changes in brachial artery were: (1) not related to blood pressure changes; (2) positively related to age, and (3) negatively correlated with baseline intracellular sodium content.
                These results suggest that moderate low-salt restriction is capable of decreasing blood pressure and peripheral resistance in carotid and forearm circulation. The increase in brachial, but not carotid, artery diameter following salt restriction suggests a difference in salt dependence among different arteries. We determined the temporal effects of dietary sodium restriction on large elastic artery compliance and systolic blood pressure (SBP) in 12 untreated, older (64+/-2 years) men and women (6 each) with stage 1 systolic hypertension. After baseline measurements subjects were assigned to 4 weeks of low or normal sodium intake (randomized, crossover design). Urinary sodium excretion was reduced by 60% by the end of week 1 of sodium restriction (54+/-11 mmol/d, P<0.01) versus baseline (135+/-14). Compared with baseline (0.11+/-0.01 mm/mm Hg), carotid artery compliance was increased by 27% (to 0.14+/-0.02, P<0.05) at the end of week 1 of sodium restriction, attaining peak levels by week 2 (+46%, to 0.16+/-0.02, P<0.01). Similarly, supine resting brachial artery SBP was reduced by >5 mm Hg by week 1 of sodium restriction, attaining peak reductions by week 2 (-12 mm Hg, P<0.01 versus baseline). The 24-hour ambulatory SBP was approximately 3 mm Hg lower at week 1 of sodium restriction and approximately 6 mm Hg lower by week 2 (P<0.01 versus baseline). The reductions in resting SBP from baseline to week 2 of sodium restriction were strongly related to the corresponding increases in carotid compliance (r=0.80, P<0.01). Urinary sodium excretion, carotid artery compliance, and SBP were not different during normal sodium intake versus baseline. Other subject characteristics were not different across conditions. Sodium restriction rapidly improves large elastic artery compliance in older adults with stage 1 systolic hypertension. These improvements in central arterial compliance appear to be a key mechanism in the rapid normalization of SBP by sodium restriction in these patients. To assess the effects of 80 mmol/day reduction in dietary sodium intake on clinic and 24-h ambulatory blood pressure in elderly hypertensive subjects.
                Double-blind, randomized, placebo-controlled, crossover trial lasting 10 weeks, following a 4-week run-in period.
                Seventeen untreated subjects with essential hypertension [systolic blood pressure (SBP) > or = 160 mmHg and/or diastolic blood pressure (DBP) > or = 95 mmHg], mean age 73 years (range 66-79).
                Subjects had clinic blood pressure and 24-h urinary electrolyte excretion measured while on their normal diet. Following a 4-week run-in period on a reduced-sodium diet (80-100 mmol/24 h) subjects entered a 10-week crossover trial of 80 mmol/24 h sodium supplement or matching placebo while continuing on the reduced-sodium diet.
                The within-patient change in clinic and 24-h ambulatory blood pressures at the end of each intervention period.
                Mean urinary sodium excretion at the end of the run-in phase rose during the high sodium intake phase and was reduced significantly at the end of the low sodium intake phase. There was a significant reduction in clinic supine SBP between the high- and low-sodium phases. There was no significant change in standing SBP, supine or standing DBP or pulse rate between phases. There was a non-significant reduction in mean 24-h SBP and DBP on the low sodium intake. At the end of the low-sodium phase there was a significant increase in plasma renin activity and aldosterone levels, but no change in plasma electrolytes.
                Overall, moderate sodium restriction in elderly hypertensives resulted in a significant fall in clinic supine SBP only, although marked differences in intersubject responses were found. Moderate sodium restriction may be of benefit in only some elderly hypertensive subjects as part of a non-pharmacological regimen for blood pressure reduction. The effects of severe and moderate sodium restriction on blood pressure, neurohormonal activity and serum lipids were studied in non-obese normotensive adults.
                In the first part of the study, 163 subjects were randomly assigned to a diet of 20 or 300 mmol/day sodium for 1 week each. In the second part, 25 subjects were given a diet of 85 or 200 mmol/day sodium for 4 weeks each in random order.
                After severe salt restriction 19% of the subjects had a significant decline (salt-sensitive group), 15% showed a significant rise (counter-regulator group) and 66% exhibited no change in blood pressure (salt-resistant group). Severe sodium restriction increased plasma renin activity and noradrenaline concentration, as well as serum total and low-density lipoprotein-cholesterol and triglycerides. After correction for haematocrit, only the changes in total and low-density lipoprotein-cholesterol remained significant. The rise in plasma renin activity during salt restriction was steeper in the counter-regulator group than in the other groups, whereas the changes in plasma noradrenaline concentrations were similar in all groups. During moderate salt restriction, plasma renin activity and noradrenaline concentration were significantly increased, but serum lipid concentrations and blood pressure did not change.
                In non-obese normotensive adults, severe and moderate salt restriction stimulates neurohormonal activity. In contrast to severe salt restriction, a moderate reduction in dietary salt intake does not influence blood lipids in normotensive subjects.
A modest reduction in salt intake for 4 or more weeks causes significant and, from a population viewpoint, important falls in BP in both hypertensive and normotensive individuals, irrespective of sex and ethnic group. With salt reduction, there is a small physiological increase in plasma renin activity, aldosterone and noradrenaline. There is no significant change in lipid levels. These results provide further strong support for a reduction in population salt intake. This will likely lower population BP and, thereby, reduce cardiovascular disease. Additionally, our analysis demonstrates a significant association between the reduction in 24-h urinary sodium and the fall in systolic BP, indicating the greater the reduction in salt intake, the greater the fall in systolic BP. The current recommendations to reduce salt intake from 9-12 to 5-6 g/d will have a major effect on BP, but are not ideal. A further reduction to 3 g/d will have a greater effect and should become the long term target for population salt intake.