OBJECTIVE: Epidemiologic evidence suggests that high levels of salt consumption are associated with "spastic" disorders of smooth muscles, ie, essential hypertension and bronchial asthma. Experimentally, it has been shown that high intake of salt leads to increased bronchial hyperreactivity in asthmatics, ie, enhanced contractility of bronchial muscle to spasmogenic stimuli. On the basis of these observations, the following questions were asked: (1) Does salt loading worsen the clinical and functional findings in asthmatics? (2) Is it the sodium or the chloride in salt that is important? METHODS: To answer these questions, the effect of salt restriction (= 5 to 6 g NaCl/d = 86 to 103 mmol Na), salt loading (+ 6.1 +/- 2.8 g NaCl/d = + 105 +/- 48 mmol Na), and loading with sodium citrate in nearly equimolar concentrations (+ 140 +/- 40 ml Shohl's solution, = + 120 +/- 30 mmol Na) was investigated in 14 asthmatics in a controlled crossover study. The total sodium load during the high salt diet was 191 to 209 mmol of sodium per day and during the sodium-citrate phase, 206 to 223 mmol of sodium per day. RESULTS: Statistical analysis showed that salt loading worsened symptoms (p = 0.06) and increased the use of inhaled steroids (p < 0.05). The effect on lung function was less equivocal: salt loading worsened the forced expiratory volume in 1 s (p < 0.01) and the peak expiratory flow rate (p < 0.05). This effect was presumably mediated by sodium, not chloride, as is demonstrated by loading with sodium citrate. CONCLUSION:Patients with bronchial asthma seems to be salt-sensitive, the responsible ion being presumably sodium. A low-salt diet appears to have a favorable effect in patients with asthma and to reduce the need for anti-asthma drugs.
RCT Entities:
OBJECTIVE: Epidemiologic evidence suggests that high levels of salt consumption are associated with "spastic" disorders of smooth muscles, ie, essential hypertension and bronchial asthma. Experimentally, it has been shown that high intake of salt leads to increased bronchial hyperreactivity in asthmatics, ie, enhanced contractility of bronchial muscle to spasmogenic stimuli. On the basis of these observations, the following questions were asked: (1) Does salt loading worsen the clinical and functional findings in asthmatics? (2) Is it the sodium or the chloride in salt that is important? METHODS: To answer these questions, the effect of salt restriction (= 5 to 6 g NaCl/d = 86 to 103 mmol Na), salt loading (+ 6.1 +/- 2.8 g NaCl/d = + 105 +/- 48 mmol Na), and loading with sodium citrate in nearly equimolar concentrations (+ 140 +/- 40 ml Shohl's solution, = + 120 +/- 30 mmol Na) was investigated in 14 asthmatics in a controlled crossover study. The total sodium load during the high salt diet was 191 to 209 mmol of sodium per day and during the sodium-citrate phase, 206 to 223 mmol of sodium per day. RESULTS: Statistical analysis showed that salt loading worsened symptoms (p = 0.06) and increased the use of inhaled steroids (p < 0.05). The effect on lung function was less equivocal: salt loading worsened the forced expiratory volume in 1 s (p < 0.01) and the peak expiratory flow rate (p < 0.05). This effect was presumably mediated by sodium, not chloride, as is demonstrated by loading with sodium citrate. CONCLUSION:Patients with bronchial asthma seems to be salt-sensitive, the responsible ion being presumably sodium. A low-salt diet appears to have a favorable effect in patients with asthma and to reduce the need for anti-asthma drugs.