Postprandial effects of a high salt meal on serum sodium, arterial stiffness, markers of nitric oxide production and markers of endothelial function
Introduction
There is substantial evidence of the adverse effects of high sodium intakes on blood pressure and cardiovascular health [1], [2]. Accumulating evidence suggests that there are adverse effects of a high sodium intake on endothelial function that are independent of blood pressure [3]. Endothelial dysfunction is regarded as an important initial event in atherogenesis and impaired nitric oxide (NO) production is thought to be a common pathway of endothelial injury and progression to clinical cardiovascular disease (CVD) [4], [5].
Endothelium dependent dilatation and endothelial NO production have been shown to be impaired by short term high salt intakes [6], [7], [8]. We previously demonstrated that flow-mediated dilatation (FMD), a measure of endothelium dependent vasodilatation, is significantly impaired after a meal containing 65 mmol Na compared with a meal containing 5 mmol Na/day but whether NO concentrations are altered following a high salt meal had not been demonstrated [9].
Arterial stiffness, a predictor of cardiovascular risk and mortality has been shown to improve with salt reduction [10], [11], [12]. However the postprandial effects of a high salt meal on measures of vascular stiffness as measured by augmentation index (AIx) it is unknown.
Elevated circulating levels of endothelin-1 (ET-1) are a hallmark of endothelial dysfunction. Chronic excess dietary sodium intake has been shown to increase ET-1 expression but it is not known if ET-1 is altered acutely by a high sodium meal [13]. Studies also suggest that inflammatory markers such as C-reactive protein (CRP) are associated with higher dietary sodium intakes in hypertensive individuals but it is not known if CRP is altered in response to a high salt meal [14].
Both AVP and atrial natriuretic peptide (ANP) have vasoactive properties and may be altered acutely following a salt load, which may in part explain the effects observed on postprandial vascular function in response to salt loading [15], [16].
Our aim was to determine if a meal containing 65 mmol Na, a sodium load which we have previously shown impairs flow-mediated dilatation [9] causes a reduction in plasma nitrate/nitrite concentrations (an index of nitric oxide production). We hypothesised sodium concentrations would increase and that nitrate/nitrite concentrations would decrease following a high salt meal. Secondary aims were to investigate the effects of the high salt meal on vascular function as measured by AIx and on plasma AVP, ANP, endothelin-1 and CRP.
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Subjects
Sixteen men and women aged between 18 and 70 years were recruited by advertisement at the local university and hospital and from the Commonwealth Scientific and Industrial Research Organisation (CSIRO) Food and Nutritional Sciences Adelaide. Inclusion criteria were body mass index (BMI) ≥18 kg/m2 and ≤27 kg/m2, systolic blood pressure (SBP) <130 mmHg, diastolic blood pressure (DBP) <90 mmHg, weight stable in the preceding 6 months, no use of anti-hypertensive medication, systemic steroids,
Subjects
Sixteen participants completed the protocol. There were no significant differences between any fasting clinical and biochemical variables between treatments (Table 1).
Biochemical parameters
The high sodium meal increased serum sodium concentration within 60 min compared with the low sodium meal (HSM 141 ± 1.3 mmol; LSM 139.6 ± 1.3 meal × time interaction p = 0.008). Serum chloride (HSM 106.7 ± 2.7 mmol; LSM 104.3 ± 1.8 mmol; meal × time interaction p = 0.002) and osmolality (HSM 294 ± 3.9mOsmol/kg; LSM
Discussion
This study demonstrated that a meal containing 65 mmol sodium raised postprandial sodium by 1.5 mmol/l in a group of healthy normotensive adults. We have previously shown that administration of a similar sodium load in a group of healthy normotensive individuals impaired postprandial flow-mediated dilatation, a nitric oxide-dependant response, within 60 min [9]. We hypothesised that the mechanism responsible for this observation would be a rise in postprandial serum sodium and a concomitant
Author responsibilities
KMD designed the protocol, conducted the study, analysed the data and wrote the manuscript. PMC and JBK designed the study, contributed to interpretation of the data and critically reviewed the manuscript. LMB contributed to study design, interpretation of the data and critically reviewed the manuscript. PHRB contributed to statistical analysis, interpretation of the data and critically reviewed the manuscript.
Funding source
Supported by the Commonwealth Scientific and Industrial Research Organisation (CSIRO) and the National Health and Medical Research Council (NHMRC) grants (44102557) (1004380) (990156) (566947).
KMD is supported by Postgraduate Scholarships from the Faculty of Health Science, University of Adelaide and the (CSIRO).
PHRB is a NHMRC Senior Research Fellow; PMC is a NHMRC Principal Research Fellow, JBK is supported by a South Australian Cardiovascular Research Development Program Research Fellowship.
Disclosures
None of the authors had any conflict of interest in relation to this manuscript.
Acknowledgements
We would like to acknowledge Vanessa Russell who contributed to the nitrate/nitrite analysis, Carlee Schultz who performed the endothelin-1 analysis and Kirsty Turner who assisted with the vascular measurements.
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