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Objective: To determine the effects of longer term modest salt reduction on blood pressure, hormones, and lipids., Design: Systematic review and meta-analysis., Data Sources: Medline, Embase, Cochrane Hypertension Group Specialised Register, Cochrane Central Register of Controlled Trials, and reference list of relevant articles., Inclusion Criteria: Randomised trials with a modest reduction in salt intake and duration of at least four weeks., Data Extraction and Analysis: Data were extracted independently by two reviewers. Random effects meta-analyses, subgroup analyses, and meta-regression were performed., Results: Thirty four trials (3230 participants) were included. Meta-analysis showed that the mean change in urinary sodium (reduced salt v usual salt) was -75 mmol/24 h (equivalent to a reduction of 4.4 g/day salt), and with this reduction in salt intake, the mean change in blood pressure was -4.18 mm Hg (95% confidence interval -5.18 to -3.18, I(2)=75%) for systolic blood pressure and -2.06 mm Hg (-2.67 to -1.45, I(2)=68%) for diastolic blood pressure. Meta-regression showed that age, ethnic group, blood pressure status (hypertensive or normotensive), and the change in 24 hour urinary sodium were all significantly associated with the fall in systolic blood pressure, explaining 68% of the variance between studies. A 100 mmol reduction in 24 hour urinary sodium (6 g/day salt) was associated with a fall in systolic blood pressure of 5.8 mm Hg (2.5 to 9.2, P=0.001) after adjustment for age, ethnic group, and blood pressure status. For diastolic blood pressure, age, ethnic group, blood pressure status, and the change in 24 hour urinary sodium explained 41% of the variance between studies. Meta-analysis by subgroup showed that in people with hypertension the mean effect was -5.39 mm Hg (-6.62 to -4.15, I(2)=61%) for systolic blood pressure and -2.82 mm Hg (-3.54 to -2.11, I(2)=52%) for diastolic blood pressure. In normotensive people, the figures were -2.42 mm Hg (-3.56 to -1.29, I(2)=66%) and -1.00 mm Hg (-1.85 to -0.15, I(2)=66%), respectively. Further subgroup analysis showed that the decrease in systolic blood pressure was significant in both white and black people and in men and women. Meta-analysis of data on hormones and lipids showed that the mean change was 0.26 ng/mL/h (0.17 to 0.36, I(2)=70%) for plasma renin activity, 73.20 pmol/L (44.92 to 101.48, I(2)=62%) for aldosterone, 187 pmol/L (39 to 336, I(2)=5%) for noradrenaline (norepinephrine), 37 pmol/L (-1 to 74, I(2)=12%) for adrenaline (epinephrine), 0.05 mmol/L (-0.02 to 0.11, I(2)=0%) for total cholesterol, 0.05 mmol/L (-0.01 to 0.12, I(2)=0%) for low density lipoprotein cholesterol, -0.02 mmol/L (-0.06 to 0.01, I(2)=16%) for high density lipoprotein cholesterol, and 0.04 mmol/L (-0.02 to 0.09, I(2)=0%) for triglycerides., Conclusions: A modest reduction in salt intake for four or more weeks causes significant and, from a population viewpoint, important falls in blood pressure in both hypertensive and normotensive individuals, irrespective of sex and ethnic group. Salt reduction is associated with a small physiological increase in plasma renin activity, aldosterone, and noradrenaline and no significant change in lipid concentrations. These results support a reduction in population salt intake, which will lower population blood pressure and thereby reduce cardiovascular disease. The observed significant association between the reduction in 24 hour urinary sodium and the fall in systolic blood pressure, indicates that larger reductions in salt intake will lead to larger falls in systolic blood pressure. The current recommendations to reduce salt intake from 9-12 to 5-6 g/day will have a major effect on blood pressure, but a further reduction to 3 g/day will have a greater effect and should become the long term target for population salt intake.

Objective: To compare the blood pressure responses of men with hypertension consuming low-sodium (Na) metabolic diets differing in dietary calcium (Ca) for two 6-week periods., Subjects: White men who had hypertension, were nonsmokers, and were sedentary., Intervention: This study consisted of two separate 6-week metabolic feeding periods. In the first period, a high-Ca group (n = 6) was fed 1,400 mg Ca per day. In the second period, a low-Ca group (n = 5) was fed 400 mg Ca per day. Both groups were fed 1,500 mg Na per day., Main Outcome Measures: Blood pressure; urine and blood measured for electrolyte, calcitriol, renin, and parathyroid hormone (PTH) levels. To measure typical nutrient intakes, 3-day dietary records were collected before the beginning of each treatment period., Statistical Analyses Performed: Repeated-measures analysis of variance and split-plot analysis of variance were used to analyze, respectively, blood pressure responses and response variables over time., Results: In both groups, serum Na level decreased (P < .05) over the 6-week period; urine Na decreased (P < .05) only in the low-Ca group. Serum PTH level decreased (P < .05) in the high-Ca group and increased (P < .05) in the low-Ca group; no change occurred in serum calcitriol level. Diastolic blood pressure decreased (8 mm Hg) in the low-Ca group (P < .05). The low-Ca group showed an 8% to 9% decrease in both systolic and diastolic blood pressure vs a 2% to 3% decrease in the high-Ca group. We also examined how the metabolic diet differed from subjects' typical diet. Results showed a positive correlation between the change in Na intake (usual to metabolic diet) and the change in systolic and diastolic blood pressure in both groups (P < .04). Results also showed a negative correlation between the change in the ratio of Na to Ca (usual to metabolic diet) and the change in diastolic blood pressure in the low-Ca group (P < .03). Directional change in blood pressure (either increase or decrease) could be predicted on the basis of how much the Na and Ca in the metabolic diet differed from subject's typical diet., Applications: Results of this study suggest that in the dietary management of hypertension it may be more important to focus on specific changes in a person's diet (eg, decreasing Na intake by 1,000 mg/day and increasing Ca intake by 400 mg/day) rather than setting specific levels of Na and Ca to be consumed.

This investigation aimed at examing the hypothesis that furosemide elicits renal sympathoexcitation through stimulation of renal renin release, which in turn produces increased plasma angiotensin II levels, causing centrally mediated sympathoexcitation. In addition, direct central nervous actions of furosemide on central control of mean arterial pressure, heart rate, and efferent renal sympathetic nerve activity were examined. Furosemide (300 mg/kg intravenously) was administered to four groups of rats: (1) control; (2) nephrectomized; (3) with intravenous losartan blockade (10 mumol/kg); and (4) with intracerebroventricular losartan blockade (10 nmol). In a fifth group of rats, furosemide was administered intracerebroventricularly (0, 2.5, 25 or 250 micrograms). To eliminate reflex control of mean arterial pressure, heart rate and efferent renal sympathetic nerve activity, all experiments were performed in rats with sinoaortic denervation and bilateral vagotomy. Experiments were performed during Saffan anaesthesia (0.9% alphaxalone/0.3% alphadolone), and rats were paralyzed with pancuronium and artifically ventilated. Furosemide produced an immediate 40% increase in efferent renal sympathetic nerve activity while the furosemide vehicle, 2 vol.% ethanolamine, did not affect efferent renal sympathetic nerve activity. The furosemide-induced increase in efferent renal sympathetic nerve activity was abolished in rats with bilateral nephrectomy but it was not affected by intravenous or intracerebroventricular losartan blockade. Intracerebroventricular angiotensin II produced an increase in mean arterial pressure and efferent renal sympathetic nerve activity whereas intravenous angiotensin II produced a pressor response in absence of increased efferent renal sympathetic nerve activity. Losartan effectively blocked responses to intravenous or intracerebroventricular angiotensin II. Intracerebroventricular administration of furosemide produced no changes in mean arterial pressure, heart rate or efferent renal sympathetic nerve activity.(ABSTRACT TRUNCATED AT 250 WORDS)