Double-blind randomised trial of modest salt restriction in older people. Adjunctive effect of salt restriction on antihypertensive efficacy. Arterial effects of salt restriction in hypertensive patients. A 9-week, randomized, double-blind, crossover study. Divergent hemodynamic and hormonal responses to varying salt intake in normotensive subjects. Effects of a low-salt diet on flow-mediated dilatation in humans. Is low salt dietary advice a useful therapy in hypertensive patients with poorly controlled blood pressure? Salt restriction among hypertensive patients: modest blood pressure effect and no adverse effects. A pilot study to test the feasibility of salt restriction in a community. Metabolic effects of strict salt restriction in essential hypertensive patients.
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 dietary salt restriction on blood pressure was measured in patients with moderate hypertension receiving antihypertensive medication. Patients were studied during a randomly allocated 6 week period of moderate dietary salt restriction and during a 6 week period of normal diet. Twenty-four of twenty-eight patients achieved a reduction of salt excretion exceeding 20%. In these patients mean urinary sodium excretion fell from 169 (s.e.m. = 13) mmol/24 h to 92 (s.e.m. = 7) mmol/24 h. Potassium excretion and body weight did not change, and with the exception of the erect systolic pressure, there was no overall change in blood pressure. When the data were grouped according to the patient medication, mean supine systolic pressure fell from 148.9 (s.e.m. = 4.4) to 140.3 (s.e.m. = 5.0) mmHg (n = 14, P greater than 0.05) and mean supine diastolic pressure fell from 100.8 (s.e.m. = 2.9) to 97.0 (s.e.m. = 2.8) mmHg (n = 14, P greater than 0.05) in patients taking diuretics. Blood pressure did not change in patients whose medication did not include diuretics. Moderate dietary salt restriction may be therapeutically useful in patients with moderate hypertension treated with diuretics but is of little value in those not receiving diuretics. 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. Blood pressure responses to 1 week of low-salt (20 mmol sodium/d) and high-salt (300 mmol sodium/d) intake were investigated in a single-blind randomized study in 163 white, nonobese normotensive subjects (65 women and 98 men; mean age, 38 +/- 1.2 years). The individuals were classified as salt sensitive when mean arterial blood pressure rose by at least 5 mm Hg during high-salt intake, as salt resistant when mean arterial blood pressure changed by less than 5 mm Hg, and as "counterregulator" when mean arterial blood pressure fell by at least 5 mm Hg during the high-salt diet. Reexamination of 31 subjects showed that this approach to the testing of salt sensitivity was reliable and reproducible. Thirty subjects (18.4%) were classified as salt sensitive, 108 (66.3%) as salt resistant, and 25 (15.3%) as counterregulators. Multiple regression analysis revealed that age, body weight, and family history of hypertension contributed significantly to the change in blood pressure after the diets. Salt sensitivity was more frequent in older subjects and in those with a positive family history of hypertension. An increase in blood pressure after salt restriction was more likely in younger individuals and in those with a negative family history of hypertension. Plasma renin activity and plasma aldosterone concentrations were lower in salt-sensitive compared with salt-resistant and counterregulating subjects. The rise in plasma renin activity during salt restriction was most pronounced in counterregulating subjects. Plasma norepinephrine concentrations were not different among the groups.(ABSTRACT TRUNCATED AT 250 WORDS) The effect of salt reduction on vascular function, assessed by brachial artery flow-mediated dilatation (FMD), is unknown.
                Our aim was to compare the effects of a low-salt (LS; 50 mmol Na/d) diet with those of a usual-salt (US; 150 mmol Na/d) diet on FMD.
                This was a randomized crossover design in which 29 overweight and obese normotensive men and women followed an LS diet and a US diet for 2 wk. Both diets had similar potassium and saturated fat contents and were designed to ensure weight stability. After each intervention, FMD, pulse wave velocity, augmentation index, and blood pressure were measured.
                FMD was significantly greater (P = 0.001) with the LS diet (4.89 +/- 2.42%) than with the US diet (3.37 +/- 2.10%), systolic blood pressure was significantly (P = 0.02) lower with the LS diet (112 +/- 11 mm Hg) than with the US diet (117 +/- 13 mm Hg), and 24-h sodium excretion was significantly lower (P = 0.0001) with the LS diet (64.1 +/- 41.3 mmol) than with the US diet (156.3 +/- 56.7 mmol). There was no correlation between change in FMD and change in 24-h sodium excretion or change in blood pressure. No significant changes in augmentation index or pulse wave velocity were observed.
                Salt reduction improves endothelium-dependant vasodilation in normotensive subjects independently of the changes in measured resting clinic blood pressure. These findings suggest additional cardioprotective effects of salt reduction beyond blood pressure reduction. The trial is registered with the Australian and New Zealand Clinical Trials Registry (unique identifier: ANZCTR12607000381482; http://www.anzctr.org.au/trial_view.aspx?ID=82159). In order to decide whether or not to advise a low Na trial routinely in a hypertension clinic, a randomised controlled 'management' trial was conducted to assess dietary compliance, well-being and changes in antihypertensive medication as a result of such a diet. Sixty-five out-patients on drug treatment for hypertension but with diastolic blood pressures greater than 95 mm Hg on two successive occasions were randomly allocated either to an index group on a 1 g Na (44 mmol) daily diet or to a reference group. Dietary advice was given in detail and repeated as necessary to ensure there was no misunderstanding. After three months 28% of the index group still added salt to their cooking and 13% sometimes added salt at the table. The difference between the groups in 24-hour Na excretion averaged 59 mmol at the end of the trial but 55% of the index group had a 24-hour Na excretion greater than 80 mmol. The average blood pressure at the end of the trial was only a 4 mm Hg systolic and 3 mm Hg diastolic lower in the index group. However, this modest benefit was achieved without any obvious deterioration in the quality of the lives of the patients on the low Na diet. The index group enjoyed their food as much as before and tended to require less drug treatment. On the debit side the index group complained more of transient unsteadiness (p less than 0.05) suggestive of postural hypotension. Low salt dietary advice is only marginally effective in patients poorly controlled on drug treatment. Non-compliance limits the usefulness of the advice. Previous studies, mainly evaluating short-term very low salt diets, suggest that salt restriction may influence glucose and insulin metabolism, catecholamines, renin, aldosterone, and lipid levels adversely. The authors wanted to explore whether sodium restriction for eight weeks influenced insulin secretion unfavourably, and evaluate the efficacy and safety of such treatment also in terms of other parameters important in the management of hypertensive patients.
                A double-blind randomized controlled parallel group designed trial. All participants received dietary advice aimed at a moderate salt-restricted diet. Half of the participants received salt capsules, the others received identical placebo capsules.
                General practice.
                Forty-six hypertensive patients inadequately controlled by drug treatment.
                Fasting serum insulin C-peptide and glucose and levels of these measures after oral glucose, blood pressure, serum aldosterone and lipids, peripheral resistance, and skin conductance.
                Salt restriction did not influence glucose and insulin metabolism, aldosterone, or lipid levels adversely. We observed better blood pressure regulation in the low salt group than in the high salt group, with a systolic and diastolic blood pressure difference of 5/5 mmHg after eight weeks. The difference was only statistically significant for diastolic blood pressure, p 0.02.
                This study revealed a modest diastolic blood pressure reducing effect of moderate sodium restriction. This reduction was obtained without any apparent unfavourable side effects such as increased insulin secretion, impaired glucose tolerance or dyslipidaemia. Index subjects were selected from the population of Milton studied in the May 1981 survey. Index subjects aged 64 or less with a systolic blood pressure 138-179 mmHg (18.35/23.8 kPa), including those on antihypertensive treatment, were invited to participate with their families. Index subjects were divided into two matched groups. One group was randomly assigned to be the control group and the other to be the salt-restriction group. Age, weight, height and 24-hour urinary excretion of sodium, potassium and creatinine at the start of the study in August 1981 were similar for the control and salt-restriction groups. When tested in November 1981, the salt-restriction group had achieved a reduction in 24-hour sodium excretion to a mean of 84 mmol for men and 70 mmol for women; corresponding values for the control groups were 150 and 120 mmol. A further test in March 1982 showed little further change. Potassium output changed very little. Attitudes to the low-salt diet varied, but 87 percent found it tolerable or actually preferable. There is no doubt that major reductions in sodium intake are feasible. However, if these are to be achieved on a large scale, food, manufacturers will need to offer a variety of low-sodium foods. Some observations suggest that a strict low-salt diet may induce unfavourable metabolic side-effects. The main aim of this study was to analyse the possible consequences of severe salt restriction in mildly hypertensive patients.
                The study was carried out through a randomized double-blind protocol.
                Forty-seven ambulatory patients proceeding from the hypertension unit were initially admitted: 17 were lost, and 30 non-diabetic mildly hypertensives (DBP 90-104 mmHg) with normal renal function completed the protocol.
                After a wash-out period, patients were maintained on a low-salt intake (2.8 +/- 1.0 g day-1 of NaCl) and placebo for 2 weeks, and the same diet and salt supplements (11.7 +/- 2.5 g day-1 of NaCl) for another 2 weeks, separated by a second wash-out period.
                At the end of each dietary period, blood pressure (BP) and body weight were measured, and a blood sample was taken for determination of routine serum chemistries, plasma lipid and apolipoprotein concentrations, immunoreactive insulin (IRI), and plasma renin activity (PRA). Urinary 24 h excretion of sodium and potassium were measured.
                During the salt restriction period BP did not change, weight lowered, and PRA raised. There was a significant increase in serum level of creatinine, uric acid, IRI, total cholesterol and apo B, and a decrease in HDL cholesterol and apo A-I.
                As previously suggested, these observations seem to indicate that strict salt restriction may cause, at least in the short-term, adverse metabolic changes in hypertensive patients.
Despite collating more event data than previous systematic reviews of randomised controlled trials (665 deaths in some 6,250 participants), there is still insufficient power to exclude clinically important effects of reduced dietary salt on mortality or cardiovascular morbidity in normotensive or hypertensive populations. Our estimates of benefits from dietary salt restriction are consistent with the predicted small effects on clinical events attributable to the small blood pressure reduction achieved.