Increased Sodium Intake Research Articles

Sodium Intake and Cardiovascular Health

Sodium is an essential nutrient. Increasing sodium intake is associated with increasing blood pressure, whereas low sodium intake results in increased renin and aldosterone levels. Randomized controlled trials have reported reductions in blood pressure with reductions in sodium intake, to levels of sodium intake <1.5 g/d, and form the evidentiary basis for current population-wide guidelines recommending low sodium intake. Although low sodium intake (<2.0 g/d) has been achieved in short-term feeding clinical trials, sustained low sodium intake has not been achieved by any of the longer term clinical trials (>6-month duration). It is assumed that the blood pressure-lowering effects of reducing sodium intake to low levels will result in large reductions in cardiovascular disease globally. However, current evidence from prospective cohort studies suggests a J-shaped association between sodium intake and cardiovascular events, based on studies from >300 000 people, and suggests that the lowest risk of cardiovascular events and death occurs in populations consuming an average sodium intake range (3-5 g/d). The increased risk of cardiovascular events associated with higher sodium intake (>5 g/d) is most prominent in those with hypertension. A major deficit in the field is the absence of large randomized controlled trials to provide definitive evidence on optimal sodium intake for preventing cardiovascular events. Pending such trials, current evidence would suggest a recommendation for moderate sodium intake in the general population (3-5 g/d), with targeting the lower end of the moderate range among those with hypertension.

Abstract P048: Sodium Intake is Associated with Weight Status in Australian Schoolchildren Aged 4-12 Years

Introduction: A high sodium intake stimulates thirst and in turn may promote greater consumption of high energy sugary beverages, which are linked to obesity risk in children. In this study we assessed the hypothesis that sodium intake, as measured by 24-hr urinary sodium excretion, would be positively associated with weight status in primary school-aged children. Methods: Cross-sectional study completed within a convenience sample of Victorian primary schools (n=43). Sodium intake was assessed via one 24-hr urine collection. Fourteen percent of samples were deemed invalid and excluded. BMI was calculated from measured weight and height and converted to BMI z-scores using the 2000 Centers for Disease Control and Prevention reference growth charts. Participants were grouped into weight categories using the International Obesity Task Force cut-points. Differences in sodium intake and weight status were assessed using multi-level linear and logistic regression analysis with adjustment for random effects (gender, age) and fixed effect (school cluster). Results: Of the 667 children with valid urine samples 55% were male and the average age was 9.3±(SD) 1.8 years. Ten percent were classified as underweight, 73% healthy weight, 14% overweight and 3% obese. Average sodium intake differed across weight categories, underweight 82±29 mmol/day (salt equivalent 4.8±1.7 g/day); healthy weight 102±43 mmol/day (salt 6.0±2.5 g/day); overweight 125±55 mmol/day (salt 7.3±3.2 g/day); obese 148±97 mmol/day (salt 8.7±5.7 g/day) (p=0.001). In the fully adjusted model sodium intake (mmol/d) was significantly associated with BMI z-score (b=0.006, P&lt;0.001). A 17 mmol/day increase in sodium intake (salt 1 g/day) was associated with a 23% (OR: 1.23; 95% CI 1.16, 1.31) greater risk of being overweight or obese, adjusted for age and gender. Conclusions: Higher sodium intake is associated with overweight and obesity in Victorian schoolchildren. This may be related to increased energy intake, and this association should be explored further.

Is complying with the recommendations of sodium intake beneficial for health in individuals at high cardiovascular risk? Findings from the PREDIMED study

Excess sodium intake is associated with high blood pressure, a major risk factor for cardiovascular disease (CVD). It is unknown whether decreasing sodium intake to <2300 mg/d has an effect on CVD or all-cause mortality. The objective was to assess whether reductions in sodium intake to <2300 mg/d were associated with either an increased or a decreased risk of fatal and nonfatal CVD and all-cause mortality. This observational prospective study of the PREvención con DIeta MEDiterránea (PREDIMED) trial included 3982 participants at high CVD risk. Sodium intake was evaluated with a validated food-frequency questionnaire and categorized as low (<1500 mg/d), intermediate (≥1500 to ≤2300 mg/d), high (>2300 to ≤3400 mg/d), or very high (>3400 mg/d). Subsequently, 1-y and 3-y changes in sodium intake were calculated. Multivariate relative risks were assessed by using Cox proportional hazards ratios. Marginal structural models with inverse probability weighting were used to test the effect of changes in sodium intake and the Mediterranean diet (MedDiet). We documented 125 CVD events and 131 deaths after a 4.8-y median follow-up. Sodium intake <2300 mg/d was associated with a lower risk of all-cause mortality: 48% (HR: 0.52; 95% CI: 0.30, 0.91; P = 0.02) and 49% (HR: 0.51; 95% CI: 0.26, 0.98; P = 0.04) after 1 and 3 y, respectively. Increasing sodium intake after 1 y was associated with a 72% (HR: 1.72; 95% CI: 1.01, 2.91; P = 0.04) higher risk of CVD events. The incidence rate of CVD was reduced for those who reduced their sodium intake and were randomly assigned to MedDiet interventions [4.1/10,000 (95% CI: 3.1, 8.0) compared with 4.4/10,000 (95% CI: 2.7, 12.4) person-years; P = 0.002]. Decreasing sodium intake to <2300 mg/d was associated with a reduced risk of all-cause mortality, whereas increasing the intake to >2300 mg/d was associated with a higher risk of CVD. Our observational data suggest that sodium intake <2300 mg/d was associated with an enhanced beneficial effect of the MedDiet on CVD. These results should be interpreted with caution, and other confirmatory studies are necessary.

Modeling of high sodium intake effects on left ventricular hypertrophy

Many clinical studies suggest that chronic high sodium intake contributes to the development of essential hypertension and left ventricular (LV) hypertrophy. In the present study, a system-level computer model has been developed to simulate the long-term effects of increased sodium intake on the LV mechanical functions and the body-fluid homeostasis. The new model couples a cardiovascular hemodynamics function model with an explicit account of the LV wall thickness variation and a long-term renal system model. The present model is validated with published results of clinical studies. The results suggest that, with increased sodium intake, the renal system function, the plasma hormone concentrations, and the blood pressure adapt to new levels of equilibrium. The LV work output and the relative wall thickness increase due to the increase of sodium intake. The results of the present model match well with the patient data.

Dairy food consumption and blood pressure among adolescents

Dairy food consumption and blood pressure among adolescents

Hypervolemia and blood pressure in prevalent kidney transplant recipients.

The prevalence and consequences of hypervolemia in kidney transplant recipients (KTRs) have not been investigated. Specifically, its impact on blood pressure (BP) and relationship with N-terminal fragment of prohormone B-type natriuretic peptide (NT-proBNP) are unknown. The objectives of this study were to establish the prevalence of hypervolemia among clinically stable KTRs, investigate the predictors of posttransplant hypervolemia, assess its impact on blood pressure, and determine its relationship with NT-proBNP. This single-center cross-sectional study enrolled 123 clinically stable KTRs. Extracellular volume status was determined by multifrequency bioimpedance analysis. Mild and severe hypervolemia were defined as percentage volume expansion of greater than 7% and greater than 15%, respectively. Systolic BP (SBP) and diastolic BP (DBP) were measured, with mean arterial pressure (MAP) calculated. Serum NT-proBNP was quantified using a noncompetitive immunoluminometric assay. Potential demographic, nutritional, and clinical predictors of extracellular volume status, BP, and NT-proBNP levels were assessed. Hypervolemia was present in 30% of KTRs, with 5% classified as severe hypervolemia. Significant predictors of volume expansion were increased sodium intake, advancing age, and reduced fat mass (P<0.01 for all associations). Hypervolemia was the only independent predictor of elevated MAP, SBP, and DBP (P<0.001 for all associations). Raised NT-proBNP levels were independently associated with both hypervolemia (P=0.01) and allograft dysfunction (P=0.03). Hypervolemia is unexpectedly common among clinically stable KTRs. It is closely associated with elevated BP. The relationship with increased sodium intake signals potential therapeutic focus. Further study is warranted to prospectively investigate objective measures of extracellular volume status among KTRs.

The effect of dietary sodium modification on blood pressure in studies of subjects with systolic blood pressure less than 140mmHg: a systematic review protocol

Review question/objective The objective of this review is to establish the effect of modifying dietary sodium intake in normotensive subjects. More specifically, the objectives are to identify the effect of reducing or increasing sodium intake on blood pressure in normotensive subjects with systolic blood pressure <140mmHg, and the effect of sodium reduction or supplementation on arterial function in subjects with baseline systolic blood pressure <140mmHg. Inclusion criteria Types of participants This review will consider studies that include adult subjects with systolic blood pressure <140mmHg and studies conducted in community settings (for example, free living populations) and controlled conditions (for example, metabolic ward, hospital and study centre). This review will exclude studies that include subjects prescribed antihypertensive or vasoactive medications. Types of interventions This review will consider studies that evaluate dietary sodium intake for equal to or greater than four weeks duration. This review will consider studies that include two study arms comprising of different levels of sodium intake. This review will consider studies that modify sodium intake via dietary modification, salt reduction, and/or salt supplementation. Types of outcomes This review will consider studies that include the following outcome measures: systolic blood pressure, diastolic blood pressure, pulse wave velocity, pulse wave analysis, and flow mediated dilatation by Doppler ultrasound.

Increased salt intake during early ontogenesis lead to development of arterial hypertension in salt-resistant Wistar rats

A direct relationship exists between salt consumption and hypertension. Increased sodium intake does not automatically lead to a rise in blood pressure (BP) because of marked intra-individual variability in salt sensitivity. Wistar rats are a salt-resistant strain and increased salt intake in adults does not induce hypertension. Mechanisms regulating BP develop during early ontogenesis and increased sodium consumption by pregnant females leads to an increase in BP of their offspring, but early postnatal stages have not been sufficiently analyzed in salt-resistant strains of rats. The aim of this work was to study the effects of increased salt during early ontogeny on cardiovascular characteristics of Wistar rats. We used 16 control (C; 8 males + 8 females) rats fed with a standard diet (0.2% sodium) and 16 experimental (S; 8 males + 8 females) rats fed with a diet containing 0.8% sodium. BP was measured weekly and plasma renin activity, aldosterone and testosterone concentrations were assayed by radioimmunoassay after the experiment in 16-week-old animals. In the kidney, AT1 receptors were determined by the western blot. BP was higher in the S as compared with the C rats and did not differ between males and females. The relative left ventricle mass was increased in S as compared with C males and no differences were recorded in females. No significant differences between groups were found in hormonal parameters and AT1 receptors. Results indicate that moderately increased salt intake during postnatal ontogeny results in a BP rise even in salt-resistant rats.

Effect of Salinity on the Survival, Ions and Urea Modulation in Red-eared Slider (Trachemys scripta elegans)

To understand the tolerance to salinity and osmoregulation of the introduced Trachemys scripta elegans, the salinity stress of four groups (salinity 5 parts per thousand, 15 parts per thousand, 25 parts per thousand and control group) were conducted. Inorganic ions, osmotic pressure, glucose and aldosterone of blood and urine in T. s. elegans (BW: 125.60 +/- 19.84 g) were analyzed at 30 d, 60 d and 90 d stress. The results showed that: 1) inorganic ions concentration of blood and urine increased with ambient salinity, which indicated that high influx of ions was combined with higher outflow when exposed to saline water in T. s. elegans. However, blood aldosterone decreased with increasing salinity, which indicated that an increased sodium intake resulting in a diminished aldosterone production. However, with elapsed time, inorganic ions in urine decreased, which indicated that inorganic ions in blood would be accumulated, and Na+ and Cl- in the plasma inevitably build up to harmful levels, at last death was happening when T. s. elegans was exposed to salinity 25 during 90 d salinity stress; 2) blood osmotic pressure increased as ambient salinity increased, it would reach 400 mOsm/kg in the group of salinity 25, which was about 1.5 fold of the control group. Higher blood osmotic pressure was due to both higher blood ions and urea concentrations. There may be another mechanism to avoid an excess of NaCl together with an important loss of water using one of the end-products of nitrogen metabolism; 3) blood glucose in each group except the group of salinity 5 decreased with time elapsed and with salinity increased. Therefore, we can conclude that T. s. elegans is an osmoregulator that limits the entry of Na+ and Cl-, but can also tolerate certain degrees of increases in plasma Na+ and Cl-. When ambient salinity was lower than 15 parts per thousand, T. s. elegans can increase blood osmotic pressure by balancing the entry of NaCl with the secretion of aldosterone decreased, and by accumulating blood urea for osmoregulation effectors, and survive for at least three months. These results could provide theoretical basis for salinity tolerance and the invasion on physiological mechanism for T. s. elegans.

What level of sodium intake worsens renal outcomes?

What level of sodium intake worsens renal outcomes?

Salt loading increases the muscle sympathetic nerve activity response to upright tilt: a pilot study (1170.3)

Increased sodium intake reduces resting muscle sympathetic nerve activity (MSNA). We hypothesized that the increase in MSNA during upright tilt would be greater following a high sodium (HS) diet compared to a low sodium (LS) diet. Six healthy women (40±6[SD]yrs) were tested following a 7 day HS (5750mgNa+/day) and 7 day LS diet (1150mgNa+/day) in randomized order during the mid‐luteal phase. Blood pressures (BP, SunTech), heart rate (HR, ECG), cardiac output (Qc, C2H2 rebreathing) and MSNA (microneurography) were measured at rest, 30o and 60o head‐up tilt. Stroke volume (SV) and total peripheral resistance (TPR) were calculated. BP was similar at supine and 30o but higher at 60o following the HS when compared to LS diet. HR, Qc, SV and TPR were similar following each diet. Supine MSNA burst frequency and burst incidence (BI) respectively were lower following the HS (13±8 bursts.min‐1, 22±13 bursts.100beats‐1) than the LS diet (22±10 bursts.min‐1, 36±18 bursts.100beats‐1). The increase in BI from baseline to 60o was greater after the HS (28±4 bursts.100beats‐1) than the LS diet (22±11 bursts.100beats‐1). These preliminary results suggest a HS diet may enhance the MSNA response and increase BP during orthostasis in healthy women. This could be due to greater sympathetic vasoconstrictor reserve and/or alteration of the sympathetic baroreflex following the HS diet.

Estimation of salt intake by 24-hour urinary sodium excretion: a cross-sectional study in Yantai, China

BackgroundHigh levels of dietary sodium are associated with raised blood pressure and adverse cardiovascular health. To determine baseline salt intake, we investigated the average dietary salt intake from 24-hour urinary sodium excretion with a small sample of Yantai adults in the Shandong province of China.MethodsOne hundred ninety one adults aged 18–69 years were randomly selected from the Yantai adult population. Blood pressure, anthropometric indices and sodium excretion in a 24-hour urine collection were measured. Consumption of condiments was derived from 3-day weighted records. Completeness of urine collections was verified using creatinine excretion in relation to weight.ResultsThe mean Na and K outputs over 24 hours were 201.5 ± 77.7 mmol/day and 46.8 ± 23.2 mmol/day, respectively (corresponding to 11.8 g NaCl and 1.8 g K). Overall, 92.1% of the subjects (96.9% of men and 87.1% of women) had intakes of over 6 g salt (NaCl)/d. The main sources of salt intake from weighed condiments records were from home cooking salt (74.7%) followed by soy sauce (15.0%). Salt intake from condiments and salt excretion were weakly correlated((r = 0.20, p = 0.005).A positive linear correlation between salt intake was associated with systolic blood pressure in all adjusted and unadjusted model (r = 0.16, p = 0.01). Each 100 mmol/day increase in sodium intake was associated with a 4.0 mmHg increase in systolic blood pressure.ConclusionDietary salt intake in Yantai adults was high. Reducing the intake of table salt and soy sauce used in cooking will be an important strategy to reduce sodium intake among Yantai adults.

Effect of maternal excessive sodium intake on postnatal brain development in rat offspring

ObjectivesPostnatal brain development is affected by the in utero environment. Modern people usually have a high sodium intake. The aim of this study was to investigate the effect of sodium hyperingestion during pregnancy on the postnatal brain development of rat offspring.MethodsThe sodium-overloaded rats received 1.8% NaCl in their drinking water for 7 days during the last week of gestation. Their body weight, urine, and blood levels of sodium and other parameters were measured. Some rats were sacrificed at pregnancy day 22 and the weight and length of the placenta and foetus were measured. The cerebral cortex and hippocampus were obtained from their offspring at postnatal day 1 and at postnatal weeks 1, 2, 4, and 8. Western blot analyses were conducted with brain tissue lysates.ResultsThe sodium-overloaded animals had decreased weight gain in the last week of gestation as well as decreased food intake, increased water intake, urine volume, urine sodium, and serum sodium. There were no differences in placental weight and length. The foetuses of sodium-overloaded rats showed decreased body weight and size, and this difference was maintained postnatally for 2 weeks. In the cerebral cortex and hippocampus of the offspring, the protein levels of myelin basic protein, calmodulin/calcium-dependent protein kinase II, and brain-derived neurotrophic factor were decreased or aberrantly expressed.DiscussionThe present data suggest that increased sodium intake during pregnancy affects the brain development of the offspring.

Endothelin converting enzyme inhibition attenuates early albuminuria and late renal failure in streptozotocin induced diabetic mice

It has recently been established that a high salt diet leads to sodium storage within the skin of rats and mice. This increase in sodium in the highly vascularized skin results in macrophage infiltration and lymphangiogenesis. While dysfunction in this process has been implicated in salt sensitive hypertension, the mechanisms are poorly understood. Because vascular endothelin-1 (ET-1) is upregulated in response to a high salt diet or hypertonicity, and is a potent chemoattractant, we hypothesized that endothelial derived ET-1 mediates infiltration of immune cells into the skin during chronic high salt intake, thereby allowing sodium clearance from the skin and preventing accumulation. Our data indicate that increasing extracellular concentration of human endothelial cells by 40 mOsm with NaCl, similar to what is seen in the interstitial space of rats placed on a high salt diet, leads to a 50% increase in ET-1 production, a mechanism likely mediated by TonEBP. Furthermore, in response to one week of high salt diet, skin Na/water ratio was elevated in vascular endothelial cell ET-1 knockout mice compared to wild type mice (0.112 ± 0.007 vs. 0.096 ± 0.004 mmol/ml). These data suggest a critical role for ET-1 in preventing the accumulation of sodium in the skin during a high salt intake, an emerging mechanism of the body's ability to buffer blood pressure changes in response to increases in sodium intake.

Salt sensitivity of renin secretion, glomerular filtration rate and blood pressure in conscious Sprague‐Dawley rats

We hypothesized that in normal rats in metabolic steady state, (i) the plasma renin concentration (PRC) is log-linearly related to Na(+) intake (NaI), (ii) the concurrent changes in mean arterial pressure (MABP) and glomerular filtration rate (GFR) are negligible and (iii) the function PRC = f(NaI) is altered by β₁-adrenoceptor blockade (metoprolol) and surgical renal denervation (DNX). In catheterized, conscious rats on low-Na(+) diet (0.004% Na(+)), NaI was increased by up to 120-fold, in four 3-day steps, by intravenous saline infusion. MABP was recorded continuously, PRC measured in arterial blood, and GFR estimated by inulin clearance. Steady states were achieved within 3 days. PRC [mIU L(-1)] was log-linearly related to NaI [mmol kg(-1) day(-1)]: PRC = -9.9 log (NaI) + 22. Set point (22 mIU L(-1) at NaI = 1) and slope (9.9 mIU per decade NaI) were independent of metoprolol administration and DNX. MABP and GFR were markedly salt-sensitive: MABP [mmHg] = 4.9 log (NaI) + 99 (P < 0.01), and GFR [mL min(-1)] = 1.4 log (NaI) + 8.3 (P < 0.01). MABP increased similarly (approx. 10%, P < 0.001) irrespective of pre-treatment. Metoprolol, but not DNX, reduced MABP, HR, and GFR (all P < 0.01). Salt sensitivity of GFR was not observed in DNX rats. Log-linear relations to sodium intake exist not only for PRC, but also for MABP and GFR, which per 10-fold increase in sodium intake rose by 5 mmHg and 1.4 mL min(-1) respectively. Steady-state levels of PRC appear independent of renal nerves. MABP and GFR seem markedly salt sensitive in normal rats.

A mathematical model of long-term renal sympathetic nerve activity inhibition during an increase in sodium intake

It is well known that renal nerves directly affect renal vascular resistance, tubular sodium reabsorption, and renin secretion. Inhibition of renal sympathetic nerve activity (RSNA) decreases renal vascular resistance, tubular sodium reabsorption, and renin secretion, leading to an increase in sodium excretion. Although several studies show that inhibition of RSNA promotes sodium excretion during an acute blood volume expansion, there is limited research relating to the importance of RSNA inhibition that contributes to sodium homeostasis during a long-term increase in sodium intake. Therefore, to dissect the underlying mechanisms of sodium excretion, a mathematical model of a cardiovascular system consisting of two kidneys, each with an independent RSNA, was developed. Simulations were performed to determine the responses of RSNA and sodium excretion to an increased sodium intake. In these simulations, RSNA in the left kidney was fixed at its normal steady-state value, while RSNA in the contralateral kidney was allowed to change normally in response to the increased sodium intake. The results demonstrate that the fixed-RSNA kidney excretes less sodium than the intact-RSNA collateral kidney. Because each kidney is exposed to the same arterial pressure and circulatory hormones, the impaired sodium excretion in the absence of RSNA inhibition supports the hypothesis that RSNA inhibition contributes to natriuresis in response to a long-term increase in sodium intake.

An Update on the Salt Wars—Genuine Controversy, Poor Science, or Vested Interest?

There is unequivocal evidence that increased sodium intake is associated with increased blood pressure, and that increased blood pressure leads to increased risk of vascular diseases. Unfortunately, the published evidence directly linking sodium intake to vascular risk is inconsistent and confusing. This review, emphasising recent developments in national and international settings, considers why this is the case and how vested interests - particularly the food industry - have exploited the vacuum. We argue that legislation is the only tool that is likely to reverse the current situation wherein many millions of lives are put at risk through an unnecessary dietary additive, the reduction of which would be eminently feasible and have no conceivable disadvantage to health.

Frequency of Hyponatremia in Gastroentric Patients Treated with Intravenous Hypotonic Fluid

How to Cite This Article: Badeli HR, Golshekan K, Shahrdami M, Azizi Asl MR, Hassanzadeh Rad A. Frequency of Hyponatremia in Gastroentric Patients Treated with Intravenous Hypotonic Fluid. J Ped. Nephrology 2013 July;1(1):23-27. Introduction : Acute gastroenteritis (AGE) is one of the most common infectious illnesses of childhood. While no treatment is needed for self-limited virus-induced AGE, dehydration caused by diarrhea and emesis is of great concern and should be treated vigorously. However, there is no consensus on the most appropriate electrolyte composition of intravenous fluids; therefore, according to basic protocols in our hospital which suggest hypotonic fluid therapy for AGE, investigators aimed to assess the frequency of hyponatremia in gastroenteritis patients treated with intravenous hypotonic fluid therapy. Materials and Methods : This descriptive observational study was conducted at 17 Shahrivar Pediatrics Hospital between September 2008 and January 2011. The patients’ medical records were assessed and children aged between 1 month and 14 years with a diagnosis of gastroenteritis and dehydration were enrolled in the study. According to sodium concentration at T0, patients were divided into three groups: hyponatremic, hypernatrmic and isonatremic. The blood samples were analyzed for the sodium concentration at T0 and during 24 hours. Statistical analyses were performed by T test and chi-square using SPSS18 and statistical significance was defined as a p-value less than 0.05. Results : The mean age of the participants was 16.43±11.1 months; 58 patients were male (67.4%) and 28 were female (32.6%). At T0, 35 patients (40.7%) were hyponatremic, 2 patients (2.3%) were hypernatremic and 49 patients were isonatremic. Sodium concentration in the hyponatremic and isonatrmic group were 137.25±1.9 and 138.29±2.04 mEq/L respectively which showed a significant difference (p=0.028). Conclusions : Our study showed that increased sodium intake could decrease acquired hyponatremia. It seems that hyponatremia could be prevented by administering high sodium concentration fluids. Keywords: Hyponatremia; Gastroenteritis; Hypotonic Solution; Intravenous Infusion

Angiotensin II Modulates Salty and Sweet Taste Sensitivities

Understanding the mechanisms underlying gustatory detection of dietary sodium is important for the prevention and treatment of hypertension. Here, we show that Angiotensin II (AngII), a major mediator of body fluid and sodium homeostasis, modulates salty and sweet taste sensitivities, and that this modulation critically influences ingestive behaviors in mice. Gustatory nerve recording demonstrated that AngII suppressed amiloride-sensitive taste responses to NaCl. Surprisingly, AngII also enhanced nerve responses to sweeteners, but had no effect on responses to KCl, sour, bitter, or umami tastants. These effects of AngII on nerve responses were blocked by the angiotensin II type 1 receptor (AT1) antagonist CV11974. In behavioral tests, CV11974 treatment reduced the stimulated high licking rate to NaCl and sweeteners in water-restricted mice with elevated plasma AngII levels. In taste cells AT1 proteins were coexpressed with αENaC (epithelial sodium channel α-subunit, an amiloride-sensitive salt taste receptor) or T1r3 (a sweet taste receptor component). These results suggest that the taste organ is a peripheral target of AngII. The specific reduction of amiloride-sensitive salt taste sensitivity by AngII may contribute to increased sodium intake. Furthermore, AngII may contribute to increased energy intake by enhancing sweet responses. The linkage between salty and sweet preferences via AngII signaling may optimize sodium and calorie intakes.

Diastolic dysfunction and arterial stiffness: the chicken or the egg

Diastolic dysfunction and arterial stiffness: the chicken or the egg