The role of caloric intake in the association of high salt intake with high blood pressure.
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SUBMITTER: Stern N
PROVIDER: S-EPMC8339119 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Background High sodium (Na+) intake is a widespread cardiovascular disease risk factor. High Na+ intake impairs endothelial function and exaggerates sympathetic reflexes, which may augment exercising blood pressure (BP) responses. Therefore, this study examined the influence of high dietary Na+ on BP responses during submaximal aerobic exercise. Methods and Results Twenty adults (8F/12M, age=24±4 years; body mass index 23.0±0.6 kg·m-2; VO2peak=39.7±9.8 mL·min-1·kg-1; systolic BP=111±10 mm Hg; diastolic BP=64±8 mm Hg) participated in this randomized, double-blind, placebo-controlled crossover study. Total Na+ intake was manipulated via ingestion of capsules containing either a placebo (dextrose) or table salt (3900 mg Na+/day) for 10 days each, separated by ?2 weeks. On day 10 of each intervention, endothelial function was assessed via flow-mediated dilation followed by BP measurement at rest and during 50 minutes of cycling at 60% VO2peak. Throughout exercise, BP was assessed continuously via finger photoplethysmography and every 5 minutes via auscultation. Venous blood samples were collected at rest and during the final 10 minutes of exercise for assessment of norepinephrine. High Na+ intake increased urinary Na+ excretion (placebo=140±68 versus Na+=282±70 mmol·24H-1; P<0.001) and reduced flow-mediated dilation (placebo=7.2±2.4 versus Na+=4.2±1.7%; P<0.001). Average exercising systolic BP was augmented following high Na+ (placebo=?30.0±16.3 versus Na+=?38.3±16.2 mm Hg; P=0.03) and correlated to the reduction in flow-mediated dilation (R=-0.71, P=0.002). Resting norepinephrine concentration was not different between conditions (P=0.82). Norepinephrine increased during exercise (P=0.002), but there was no Na+ effect (P=0.26). Conclusions High dietary Na+ augments BP responses during submaximal aerobic exercise, which may be mediated, in part, by impaired endothelial function.
| S-EPMC7660875 | biostudies-literature
Project description:So far, few studies have examined the effect of salt taste receptors genetic variation on dietary intake in the Iranian population. We aimed to evaluate associations between single nucleotide polymorphisms (SNPs) in salt taste receptors' genes with dietary salt intake and blood pressure. A cross-sectional study was carried out among 116 randomly selected healthy adults aged ≥ 18 in Isfahan, Iran. Participants underwent sodium intake determination by 24-h urine collection, as well as dietary assessment by semi-quantitative food frequency questionnaire and blood pressure measurement. Whole blood was collected to extract DNA and genotype of SNP rs239345 in SCNN1B and rs224534, rs4790151 and rs8065080 in TRPV1 gene. Sodium consumption and diastolic blood pressure were significantly higher in carriers of the A-allele in rs239345 compared to subjects with the TT genotype (4808.4 ± 824.4 mg/day vs. 4043.5 ± 989.3 mg/day; P = 0.004) and 83.6 ± 8.5 mmHg vs. 77.3 ± 7.3 mmHg; P = 0.011), respectively. The level of sodium intake was lower in the TT genotype of TRPV1 (rs224534) than the CC genotype (3767.0 ± 713.7 mg/day vs. 4633.3 ± 793.5 mg/day; P = 0.012). We could not find any association between genotypes of all SNPs with systolic blood pressure as well as genotypes of rs224534, rs4790151 and rs8065080 with diastolic blood pressure. Genetic variations can relate with salt intake and consequently may associate with hypertension and finally cardiovascular disease risk in the Iranian population.
| S-EPMC10006406 | biostudies-literature
Project description:ObjectiveTo evaluate the association of salt consumption with blood pressure in Viet Nam, a developing country with a high level of salt consumption.Design and settingAnalysis of a nationally representative sample of Vietnamese adults 25-65 years of age who were surveyed using the World Health Organization STEPwise approach to Surveillance protocol. Participants who reported acute illness, pregnancy, or current use of antihypertensive medications were excluded. Daily salt consumption was estimated from fasting mid-morning spot urine samples. Associations of salt consumption with systolic blood pressure and prevalent hypertension were assessed using adjusted linear and generalized linear models. Interaction terms were tested to assess differences by age, smoking, alcohol consumption, and rural/urban status.ResultsThe analysis included 2,333 participants (mean age: 37 years, 46% male, 33% urban). The average estimated salt consumption was 10g/day. No associations of salt consumption with blood pressure or prevalent hypertension were observed at a national scale in men or women. The associations did not differ in subgroups defined by age, smoking, or alcohol consumption; however, associations differed between urban and rural participants (p-value for interaction of urban/rural status with salt consumption, p = 0.02), suggesting that higher salt consumption may be associated with higher systolic blood pressure in urban residents but lower systolic blood pressure in rural residents.ConclusionsAlthough there was no evidence of an association at a national level, associations of salt consumption with blood pressure differed between urban and rural residents in Viet Nam. The reasons for this differential association are not clear, and given the large rate of rural to urban migration experienced in Viet Nam, this topic warrants further investigation.
| S-EPMC5773206 | biostudies-literature
Project description:BackgroundA few prospective studies have investigated the potential association of soft drink and non-caloric soft drink intake with high blood pressure using methods that adequately consider changes in intake over time and hypertensive status at baseline.ObjectiveTo prospectively examine the association of soft drink and non-caloric soft drink intake with systolic and diastolic blood pressure in a sample of Mexican adults, overall and by hypertension status.MethodsWe used data from the Health Workers Cohort Study spanning from 2004 to 2018 (n = 1,324 adults). Soft drink and non-caloric soft drink intake were assessed with a semiquantitative food frequency questionnaire. We fit multivariable-adjusted fixed-effects models to test the association of soft drink and non-caloric soft drink intake with systolic and diastolic blood pressure. The models were adjusted for potential confounders and considering the potential modifying effect of hypertension status at baseline.ResultsA one-serving increase in soft drink intake was associated with a 2.08 mm Hg (95% CI: 0.21, 3.94) increase in systolic blood pressure and 2.09 mm Hg (95% CI: 0.81, 3.36) increase in diastolic blood pressure over ten years. A stronger association between soft drink intake and diastolic pressure was observed among participants with versus without hypertension at baseline. We found no association between non-caloric soft drink intake and blood pressure.ConclusionsOur findings support the hypothesis that soft drink intake increases blood pressure. While further studies should be conducted to confirm our findings, food policies and recommendations to limit soft drink intake are likely to help reduce blood pressure at the population level. We probably did not find an association between non-caloric soft drink intake and blood pressure because of the low consumption of this type of beverage in the cohort. More studies will be needed to understand the potential effect of non-caloric beverages on blood pressure.
| S-EPMC9171938 | biostudies-literature
Project description:Blood pressure (BP) is a strong cardiovascular risk factor, predicting cardiovascular mortality in the general population. High salt consumption is a major contributor of increased BP and hypertension. However, there is a controversy on whether BP response to salt intake would be sex-specific. Thus, we aimed to verify the changes in BP according to different salt intake in men and women in a large sample of adults. The present analysis refers to 12 813 participants (from 35 to 64 years) with a validated 12-hour overnight urine collection in which salt intake was estimated. A set of questionnaires, clinical examination, and laboratory tests were carried out during a single visit to one of the six investigation centers involved. Salt intake was 12.9 ± 5.9 g/d in men and 9.3 ± 4.3 g/d in women. BP increases as salt intake increases, regardless of using BP-lowering medication. The slope of increase in BP elicited by salt intake was significantly higher in women than in men. Thus, the increase in BP by salt intake was stepper in women even after controlling for confounders, regardless of using BP-lowering medication or being hypertensive. In conclusion, salt intake is elevated in this large sample of Brazilian adults in which only a few participants are compliant with the recommendation. Also, women have a higher responsiveness of BP according to salt intake than men, and it is not associated with age, BP level, or the use of BP-lowering medication.
| S-EPMC8030395 | biostudies-literature
Project description:Abstract Objectives So far, few researches has examined how genetic variation in salt taste receptors affects food intake in Iranian population. Thus, in this study, we aimed to investigate associations of single nucleotide polymorphisms (SNPs) in salt taste receptors genes with dietary salt intake and blood pressure. Methods This cross-sectional study was carried out among 116 randomly selected adults aged 18 years and over in Isfahan city, Iran. Subjects with diabetes insipidus, renal insufficiency, a special dietary regimen, fasting or menstruating on the day of sampling, using diuretics and oral contraceptives or pregnant and lactating women as well as participants who had incomplete 24-h urine collection were excluded. A 24-h urine collection and blood pressure measurement were done. Whole blood was collected to extract DNA and measure SNP rs239345 in the ENaC and rs224534, rs4790151 and rs8065080 in the TRPV1 gene. Results Homozygous carriers of the T allele for rs239345 were found to consume significantly more sodium (4414.7 ± 1943.8 mg/day) compared to the AA genotype (3887.4 ± 1709.1 mg/day). Further, they also had higher diastolic blood pressure compared to subjects with the AA genotype (81.3 ± 9.7 vs. 75.3 ± 8.3 mmHg). Compared to subjects with the CC genotype, those with homozygous carriers of the T allele for rs8065080 in the TRPV1 had higher sodium intake (3592.6 ± 1645.2 mg/day vs. 4604.2 ± 2013.5 mg/day) and systolic blood pressure (118.1 ± 11.3 mmHg vs. 123.4 ± 11.5 mmHg). No differences were found in dietary sodium intake and blood pressure with the rs224534 and rs4790151 SNPs. Conclusions These findings suggest that genetic variation in the ENaC and TRPV1 genes may contribute to inter-individual differences in salt intake and blood pressure. Funding Sources The National Institute for Medical Research Development (NIMAD) was funded this study via grant number of 977,549.
| S-EPMC8340790 | biostudies-literature
Project description:The effect of lowering sympathetic nerve activity by renal denervation (RDN) is highly variable. With the exception of office systolic blood pressure (BP), predictors of the BP-lowering effect have not been identified. Because dietary sodium intake influences sympathetic drive, and, conversely, sympathetic activity influences salt sensitivity in hypertension, we investigated 24-hour urinary sodium excretion in participants of the SYMPATHY trial. SYMPATHY investigated RDN in patients with resistant hypertension. Both 24-hour ambulatory and office BP measurements were end points. No relationship was found for baseline sodium excretion and change in BP 6 months after RDN in multivariable-adjusted regression analysis. Change in the salt intake-measured BP relationships at 6 months vs baseline was used as a measure for salt sensitivity. BP was 8 mm Hg lower with similar salt intake after RDN, suggesting a decrease in salt sensitivity. However, the change was similar in the control group, and thus not attributable to RDN.
| S-EPMC8030930 | biostudies-literature
Project description:OBJECTIVES:The aims of this study were to test the hypothesis that short-term high salt intake reduces macrovascular and microvascular endothelial function in the absence of changes in blood pressure and to determine whether acute exercise restores endothelial function after high salt in women. MATERIALS AND METHODS:Twelve women were administered high salt (11?g of sodium chloride for 7 days) and then underwent a weightlifting session. Brachial artery flow-mediated dilation and nitroglycerin dilation were measured with ultrasound at baseline, after high salt, and after weightlifting. Subcutaneous fat tissue biopsies were obtained at baseline, after high salt, and after weightlifting. Resistance arteries from biopsies were cannulated for vascular reactivity measurements in response to flow [flow-induced dilation (FID)] and acetylcholine. RESULTS:Blood pressure was similar before and after high salt diet. Brachial flow-mediated dilation was reduced after high salt diet but was not affected by acute weightlifting. Brachial nitroglycerin dilations were similar before and after high salt. FID and acetylcholine-induced dilation of resistance arteries were similar to that of before and after high salt diet. FID and acetylcholine-induced dilation was not altered by weightlifting after high salt diet. However, N-nitro-L-arginine methyl ester significantly reduced FID at baseline and after exercise but had no effect dilator reactivity after high salt diet alone. CONCLUSION:These data suggest that high salt intake reduces brachial artery endothelial function and switches the mediator of vasodilation in the microcirculation to a non-nitric oxide-dependent mechanism in healthy adults and acute exercise may switch the dilator mechanism back to nitric oxide during high salt diet.
| S-EPMC6711169 | biostudies-literature
Project description:The mechanisms by which dietary salt promotes hypertension are unknown. Previous work established that plasma [Na(+)] and osmolality rise in proportion with salt intake and thus promote release of vasopressin (VP) from the neurohypophysis. Although high levels of circulating VP can increase blood pressure, this effect is normally prevented by a potent GABAergic inhibition of VP neurons by aortic baroreceptors. Here we show that chronic high salt intake impairs baroreceptor inhibition of rat VP neurons through a brain-derived neurotrophic factor (BDNF)-dependent activation of TrkB receptors and downregulation of KCC2 expression, which prevents inhibitory GABAergic signaling. We show that high salt intake increases the spontaneous firing rate of VP neurons in vivo and that circulating VP contributes significantly to the elevation of arterial pressure under these conditions. These results provide the first demonstration that dietary salt can affect blood pressure through neurotrophin-induced plasticity in a central homeostatic circuit.
| S-EPMC4577058 | biostudies-literature
Project description:ObjectiveCognitive factors and anticipation are known to influence food intake. The current study examined the effect of anticipation and actual consumption of food on hormone (ghrelin, cortisol, and insulin) and glucose levels, appetite and ad libitum intake, to assess whether changes in hormone levels might explain the predicted differences in subsequent food intake.Design and methodsDuring four breakfast sessions, participants consumed a yogurt preload that was either low caloric (LC: 180 kcal/300 g) or high caloric (HC: 530 kcal/300 g) and was provided with either consistent or inconsistent calorie information (i.e., stating the caloric content of the preload was low or high). Appetite ratings and hormone and glucose levels were measured at baseline (t = 0), after providing the calorie information about the preload (t = 20), after consumption of the preload (t = 40), and just before ad libitum intake (t = 60).ResultsAd libitum intake was lower after HC preloads (as compared to LC preloads; P < 0.01). Intake after LC preloads was higher when provided with (consistent) LC information (467±254 kcal) as compared to (inconsistent) HC information (346±210 kcal), but intake after the HC preloads did not depend on the information provided (LC information: 290±178 kcal, HC information: 333±179 kcal; caloric load*information P = 0.03). Hormone levels did not respond in an anticipatory manner, and the post-prandial responses depended on actual calories consumed.ConclusionsThese results suggest that both cognitive and physiological information determine food intake. When actual caloric intake was sufficient to produce physiological satiety, cognitive factors played no role; however, when physiological satiety was limited, cognitively induced satiety reduced intake to comparable levels.
| S-EPMC3817524 | biostudies-literature