***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 There is a paucity of quality evidence regarding the effects of sodium restriction in patients with CKD , particularly in patients with pre-end stage CKD , where controlling modifiable risk factors may be especially important for delaying CKD progression and cardiovascular events . We conducted a double-blind placebo-controlled r and omized crossover trial assessing the effects of high versus low sodium intake on ambulatory BP , 24-hour protein and albumin excretion , fluid status ( body composition monitor ) , renin and aldosterone levels , and arterial stiffness ( pulse wave velocity and augmentation index ) in 20 adult patients with hypertensive stage 3 - 4 CKD as phase 1 of the LowSALT CKD study . Overall , salt restriction result ed in statistically significant and clinical ly important reductions in BP ( mean reduction of systolic/diastolic BP , 10/4 mm Hg ; 95 % confidence interval , 5 to 15 /1 to 6 mm Hg ) , extracellular fluid volume , albuminuria , and proteinuria in patients with moderate-to-severe CKD . The magnitude of change was more pronounced than the magnitude reported in patients without CKD , suggesting that patients with CKD are particularly salt sensitive . Although studies with longer intervention times and larger sample sizes are needed to confirm these benefits , this study indicates that sodium restriction should be emphasized in the management of patients with CKD as a means to reduce cardiovascular risk and risk for CKD progression The role of salt restriction in patients with impaired glucose tolerance and diabetes mellitus is controversial , with a lack of well controlled , longer term , modest salt reduction trials in this group of patients , in spite of the marked increase in cardiovascular risk . We carried out a 12-week r and omized double-blind , crossover trial of salt restriction with salt or placebo tablets , each for 6 weeks , in 46 individuals with diet-controlled type 2 diabetes mellitus or impaired glucose tolerance and untreated normal or high normal blood pressure ( BP ) . From salt to placebo , 24-hour urinary sodium was reduced by 49±9 mmol ( 2.9 g salt ) . This reduction in salt intake led to fall in clinic BP from 136/81±2/1 mm Hg to 131/80±2/1 mm Hg , ( systolic BP ; P<0.01 ) . Mean ambulatory 24-hour BP was reduced by 3/2±1/1 mm Hg ( systolic BP , P<0.01 and diastolic BP , P<0.05 ) , and albumin/creatinine ratio was reduced from 0.73 mg/mmol ( 0.5–1.5 ) to 0.64 mg/mmol ( 0.3–1.1 ; P<0.05 ) . There was no significant change in fasting glucose , hemoglobin A1c , or insulin sensitivity . These results demonstrate that a modest reduction in salt intake , to approximately the amount recommended in public health guidelines , leads to significant and clinical ly relevant falls in BP in individuals who are early on in the progression of diabetes mellitus with normal or mildly raised BP . The reduction in urinary albumin excretion may carry additional benefits in reducing cardiovascular disease above the effects on BP Objective High salt intake is known to be the most pivotal environmental factor in the pathogenesis of hypertension . However , the association of high sodium intake with central hemodynamics in hypertensive individuals has not been well defined . Here , we determined the association of estimated 24-h urine sodium and potassium excretion estimated from a spot urine analysis with parameters of central pulse wave analysis in 515 hypertensive individuals . Methods Fasting spot urine sample s were obtained in the early morning after the first void , and estimated 24-h urine sodium and potassium excretion were estimated from measurement of urine sodium , potassium and creatinine .  Central hemodynamics and arterial stiffness parameters were assessed via pulse wave analysis of the radial artery . Results The estimated 24-h sodium and potassium excretion values were 150 ± 40 and 49 ± 10 mEq , respectively . There was a step-wise decrease in pulse pressure amplification with increasing estimated 24-h urine sodium excretion . Multiple linear regression analyses revealed that both estimated 24-h urine sodium excretion and sodium/potassium ratio were independently associated with increases in central pulse pressure , augmented aortic pressure and augmentation index and were inversely associated with pulse pressure amplification . Conclusion The estimated 24-h urinary sodium excretion is independently associated with central hemodynamics . This may provide the basis for prospect i ve interventional studies of epidemiologic scale to determine the potential beneficial effects of reduced salt consumption on central hemodynamics We tested the hypothesis that the Na+ component of dietary NaCl can have a pressor effect apart from its capacity to complement the extracellular osmotic activity of Cl− and , thus , exp and plasma volume . We studied 35 mostly normotensive blacks who ingested a low-NaCl diet , 30 mmol/d , for 3 weeks , in the first and third of which Na+ was loaded orally with either NaHCO3 or NaCl , in r and om order ( 250 mmol/d ) . In subjects adjudged to be salt sensitive ( n=18 ; & Dgr ; mean arterial pressure : ≥5 mm Hg with NaCl load ) , but not in salt-resistant subjects ( n=17 ) , loading with NaHCO3 was also pressor . The pressor effect of NaHCO3 was half that of NaCl :  mean arterial pressure ( millimeters of mercury ) increased significantly from 90 on low NaCl to 95 with NaHCO3 and to 101 with NaCl . The pressor effect of NaCl strongly predicted that of NaHCO3 . As judged by hematocrit decrease , plasma volume expansion  with NaCl was the same in salt-resistant and salt-sensitive subjects and twice that with NaHCO3 , irrespective of the pressor effect . In salt-sensitive subjects , mean arterial pressure varied directly with plasma Na+ concentration attained with all Na+ loading . In salt-sensitive but not salt-resistant subjects , NaHCO3 and NaCl induced decreases in renal blood flow and increases in renal vascular resistance ; changes in renal blood flow were not different with the 2 salts . Responses of renal blood flow and renal vascular resistance to NaHCO3 were strongly predicted by those to NaCl . In establishing the fact of “ sodium-selective ” salt sensitivity , the current observations demonstrate that the Na+ component of NaCl can have pressor and renal vasoconstrictive properties apart from its capacity to complement Cl− in plasma volume expansion BACKGROUND AND OBJECTIVES Systolic BP and large elastic artery stiffness both increase with age and are reduced by dietary sodium restriction . Production of the natriuretic hormone marinobufagenin , an endogenous α1 Na+,K+-ATPase inhibitor , is increased in salt-sensitive hypertension and contributes to the rise in systolic BP during sodium loading . DESIGN , SETTING , PARTICIPANTS , & MEASUREMENTS The hypothesis was that dietary sodium restriction performed in middle-aged/older adults ( eight men and three women ; 60 ± 2 years ) with moderately elevated systolic BP ( 139 ± 2/83 ± 2 mmHg ) would reduce urinary marinobufagenin excretion as well as systolic BP and aortic pulse-wave velocity ( r and omized , placebo-controlled , and crossover design ) . This study also explored the associations among marinobufagenin excretion with systolic BP and aortic pulse-wave velocity across conditions of 5 weeks of a low-sodium ( 77 ± 9 mmol/d ) and 5 weeks of a normal-sodium ( 144 ± 7 mmol/d ) diet . RESULTS Urinary marinobufagenin excretion ( weekly measurements ; 25.4 ± 1.8 versus 30.7 ± 2.1 pmol/kg per day ) , systolic BP ( 127 ± 3 versus 138 ± 5 mmHg ) , and aortic pulse-wave velocity ( 700 ± 40 versus 843 ± 36 cm/s ) were lower during the low- versus normal-sodium condition ( all P<0.05 ) . Across all weeks , marinobufagenin excretion was related with systolic BP ( slope=0.61 , P<0.001 ) and sodium excretion ( slope=0.46 , P<0.001 ) . These associations persisted during the normal- but not the low-sodium condition ( both P<0.005 ) . Marinobufagenin excretion also was associated with aortic pulse-wave velocity ( slope=0.70 , P=0.02 ) and endothelial cell expression of NAD(P)H oxidase-p47phox ( slope=0.64 , P=0.006 ) . CONCLUSIONS These results show , for the first time in humans , that dietary sodium restriction reduces urinary marinobufagenin excretion and that urinary marinobufagenin excretion is positively associated with systolic BP , aortic stiffness ( aortic pulse-wave velocity ) , and endothelial cell expression of the oxidant enzyme NAD(P)H oxidase . Importantly , marinobufagenin excretion is positively related to systolic BP over ranges of sodium intake typical of an American diet , extending previous observations in rodents and humans fed experimentally high-sodium diets We performed a r and omised , placebo-controlled , crossover study to examine the effects of sodium and potassium supplementation on  blood pressure ( BP ) and arterial stiffness in untreated (pre)hypertensive individuals . During the study , subjects were on a fully controlled diet that was relatively low in sodium and potassium . After a 1-week run-in period , subjects received capsules with supplemental sodium ( 3 g d−1 , equals 7.6 g d−1 of salt ) , supplemental potassium ( 3 g d−1 ) or placebo , for 4 weeks each , in r and om order . Fasting office BP , 24-h ambulatory BP and measures of arterial stiffness  were assessed at baseline and every 4 weeks . Of 37 r and omized subjects , 36 completed the study . They had a mean pre-treatment BP of 145/81 mm Hg and 69 % had systolic BP ⩾140 mm Hg . Sodium excretion was increased by 98 mmol per 24 h and potassium excretion by 63 mmol per 24 h during active interventions , compared with  placebo .  During sodium supplementation , office BP was significantly increased by 7.5/3.3 mm Hg , 24-h BP by 7.5/2.7 mm Hg and central BP by 8.5/3.6 mm Hg . During potassium supplementation , 24-h BP was significantly reduced by 3.9/1.6 mm Hg and central pulse pressure by 2.9 mm Hg . Pulse wave velocity and augmentation index were not significantly affected by sodium or potassium supplementation . In conclusion , increasing the intake of sodium caused a  substantial increase in BP in subjects with untreated elevated BP . 
    Output:
    
Conclusion : The results of this meta- analysis indicate that restriction of dietary sodium intake reduces arterial stiffness .
This effect seems be at least in part independent of the changes in blood pressure