***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: 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 r and omized 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 Active and inactive urinary kallikrein excretion rates were evaluated in 43 essential hypertensive men ( 45.4 + /- 5.6 yr ) after normal-(120 mmol/day ) , low-(20 mmol/day ) , and high-(240 mmol/day ) NaCl diets were given for 2 wk each . Patients were classified as salt-sensitive , salt-resistant , or counterregulating , on the basis of their blood pressure responses to the different NaCl intakes . Result ing data show that active and inactive kallikrein excretion rates were lower ( P < 0.001 ) in salt-sensitive ( active , 0.59 + /- 0.27 U/24 h ; inactive , 3.45 + /- 1.31 U/24 h ) than in salt-resistant ( active , 1.41 + /- 0.35 U/24 h ; inactive , 6.93 + /- 2.68 U/24 h ) and in counterregulating hypertensive patients ( active , 1.37 + /- 0.39 U/24 h ; inactive , 6.32 + /- 2.58 U/24 h ) after the normal NaCl diet . Salt-sensitive hypertensive patients showed also higher plasma digoxin-like substance ( P < 0.001 ) , atrial natriuretic peptide ( P < 0.001 ) , and fasting insulin ( P < 0.005 ) levels than the other subgroups . Active kallikrein decreased after high and increased after low-NaCl intake in all groups . Inactive kallikrein varied similarly to active one in salt-resistant patients and counterregulating patients , whereas it increased during salt-loading in salt-sensitive patients . Consequently , the active/total kallikrein ratio decreased in salt-sensitive patients ( from 20.2 + /- 3.5 to 5.82 + /- 1.02 % , P < 0.05 ) when they switched from low- to high-NaCl intake , and the ratio was lower in these patients than in the other subgroups ( P < 0.0001 ) after the high-NaCl diet . In conclusion , active and inactive kallikrein excretions after normal-NaCl intake are reduced in salt-sensitive hypertensive patients . The divergent active and inactive kallikrein responses to dietary NaCl changes in salt-sensitive patients could indicate an impairment of inactive to active kallikrein conversion during NaCl loading as a new mechanism in human salt-sensitive hypertension Sodium restriction can reduce blood pressure in hypertensive patients . The present study indicates that if hypertension is well controlled then the reemergence of hypertension can be decreased by the use of a reduced sodium intake . The present paper demonstrates that in such patients on a normal salt diet  , 90 % become hypertensive within 6 months while only 40 % of people on a reduced sodium diet  become hypertensive . It is proposed that a high sodium intake activates a number of amplifiers that causes a shift of the dose-response curve to sodium to the left and if not prevented or interrupted leads to the development of hypertension We sought to explore the effects of salt loading in young normotensives on vascular endothelial function , echocardiographic left ventricular diastolic function , and electrocardiographic QT dispersion .  Sixteen healthy normotensive male volunteers were r and omized in a double-blind crossover fashion to 5-day treatment periods with either placebo or salt tablets ( 200 mmol/d of sodium ) separated by a 2-week washout period . Throughout the study the volunteers were asked to maintain a low-salt diet .  Forearm venous occlusion plethysmography and intraarterial infusions  of  acetylcholine ( ACh ) , sodium nitroprusside  ( SNP ) , and NG-monomethyl-l-arginine ( L-NMMA ) were used to assess vascular reactivity . Baseline and postsalt loading 12-lead ECGs and echocardiograms were also obtained . Twenty-four-hour ambulatory systolic blood pressure rose ( 117±11 to 121±8 mm Hg ) significantly with salt loading . The endothelium-dependent responses to ACh were significantly blunted with salt compared to placebo ( & Dgr;FBF% 403 [ 50 ] versus 296 [ 31 ] ; P<0.05 ) and L-NMMA ( & Dgr;FBF% −47.2 [ 4 ] versus −31 [ 3 ] ; P<0.01 ) . In contrast , the endothelium-independent response to SNP was not different between treatments . Color M-mode flow propagation velocity ( CMMFPV ) , a preload index of left ventricular diastolic function , was significantly reduced with salt ( 64 [ 6 ] versus 59 [ 16 ] cm/s ; P<0.05 ) suggesting increased ventricular stiffness . QT dispersion was also significantly increased with salt ( 58 [ 16 ] versus 48 [ 17 ] ms ; P=0.02 ) . Salt loading impaired vascular endothelial function , left ventricular mechanical relaxation , and electric repolarization in young healthy normotensives Objective : 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 Design : Blood pressure responses were assessed in 66 subjects ( 36 male , 30 female ; mean age 65 years ) on two diets differing by approximately 70mmol/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 Results : 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 and roid 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 Conclusions : 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 The aim of this study was to determine whether moderate restriction of dietary salt intake leads to an additional fall in blood pressure in treated hypertensive men who are asked to simultaneously reduce their usual alcohol intake . Sixty-three subjects entered an initial 2-week familiarization period during which they continued their usual alcohol intake and commenced a " low sodium " diet ( less than 60 mmol/day ) supplemented with 100 mmol sodium chloride per day as enteric-coated tablets . Subjects were then r and omly assigned to either drink a low alcohol beer alone for a 4-week period ( reducing their self-reported alcohol consumption from 537 to 57 ml/week ) or to continue their usual alcohol intake ( 543 versus 557 ml/week ) . Within the low and normal alcohol intake groups , subjects were assigned to either a low or normal sodium intake . The low sodium groups continued the sodium-restricted diet but were switched to placebo sodium chloride tablets for the 4 weeks . This result ed in a fall in the 24-hour urinary sodium excretion from 144 to 69 mmol/day . The normal sodium groups continued the low sodium diet but kept taking 100 mmol/day of the sodium chloride tablets , and their urinary sodium excretion remained unchanged ( 125 versus 142 mmol/day ) . Regular antihypertensive therapy was continued throughout . Fifty-nine subjects completed the trial . In those who reduced their alcohol intake there was a fall in both systolic blood pressure ( -5.4 mm Hg supine , p less than 0.01 ) and diastolic blood pressure ( -3.2 mm Hg supine , p less than 0.01 ) . ( ABSTRACT TRUNCATED AT 250 WORDS Objectives To evaluate salt sensitivity in elderly subjects with different forms of hypertension and controls and to investigate any modulation by genotype Design R and omized , double-blinded , placebo-controlled latin-square Setting Tertiary referral hospital Participants Community subjects ( n = 46 ) aged ⩾ 60 years classified as isolated systolic hypertension [ ISH ; systolic blood pressure ( SBP ) ⩾ 160 , diastolic blood pressure ( DBP ) < 90 mmHg , n = 19 ] , diastolic ± systolic hypertension ( SDH ; DBP ⩾ 90 mmHg , n = 10 ) and normotension ( SBP < 160 , DBP < 90 mmHg , n = 17 ) .  Intervention Four 14 day treatments , 50 , 100 , 200 and 300 mmol/day of sodium chloride supplementation interspersed with 14 day washout periods on a salt-restricted diet . Main outcome measures The 24 h blood pressure , heart rate , weight , urinary sodium and creatinine clearance measured during baseline , treatment and washout periods and angiotensinogen ( AGT ) and angiotensin converting enzyme ( ACE ) genotypes . Results For the entire cohort , the mean ± st and ard error ( SE ) of change from baseline in SBP for 50 , 100 , 200 and 300 mmol/day salt was 7.7 ± 2.4 , 12.1 ± 2.4 , 16.6 ± 3.0 , 18.5 ± 2.6 mmHg , respectively . For DBP , the respective changes were:− 0.1 ± 1.5 , 2.4 ± 1.6 , 3.0 ± 1.5 , 5.8 ± 1.7 mmHg . The increase in SBP among ISH subjects was significantly higher than among subjects in the SDH and normotensive groups ( P < 0.05 ) . AGT genotype influenced the effect of salt dose on the change in DBP ( P = 0.006 ) but not SBP ( P = 0.7 ) . Conclusions In healthy , older subjects , a linear increase in BP occurred with increasing salt dose , it appeared most pronounced in ISH subjects and could be modulated by AGT genotype Summary In order to examine the effect of dietary sodium intake on plasma lipids , 15 healthy male volunteers were given a low-salt diet ( 20 mmol/day ) for 3 weeks , adding either placebo , sodium chloride ( 200 mmol/day ) , or a non-chloride sodium salt ( sodium citrate , 200 mmol Na/day ) 
    Output:
    
Reductions in blood pressure were observed in diverse population subsets examined , including hypertensive and non-hypertensive individuals .
For the same reduction in 24 hour urinary sodium there was greater SBP reduction  in older people , non-white population s , and those with higher baseline SBP levels .
Conclusions The magnitude of blood pressure lowering achieved with sodium reduction showed a dose-response relation and was greater for older population s , non-white population s , and those with higher blood pressure .
Short term studies underestimate the effect of sodium reduction on blood pressure .