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European Heart Journal Advance Access originally published online on October 17, 2007
European Heart Journal 2007 28(22):2726-2731; doi:10.1093/eurheartj/ehm396
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For permissions please email: journals.permissions@oxfordjournals.org

Altered sodium intake affects plasma concentrations of BNP but not proBNP in healthy individuals and patients with compensated heart failure

Morten Damgaard1,2,*, Jens Peter Goetze3, Peter Norsk4 and Niels Gadsbøll2,5

1 Division of Aviation Medicine, Medical Department B, Rigshospitalet, Copenhagen DK-2100, Denmark
2 Department of Cardiovascular Medicine, Bispebjerg Hospital, Bispebjerg Bakke 23,Copenhagen DK-2400 NV, Denmark
3 Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark
4 Department of Biomedical Sciences, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark
5 Department of Medicine, Køge Sygehus, Copenhagen, Denmark

Received 13 June 2006; revised 14 August 2007; accepted 24 August 2007; online publish-ahead-of-print 17 October 2007.

* Corresponding author. Tel: +45 35 45 76 97; fax: +45 35 45 76 27. E-mail address: mdamgaard{at}dadlnet.dk


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Conclusion
 Funding
 Acknowledgements
 Reference
 
Aims: Plasma B-type natriuretic peptide (BNP) and proBNP are promising markers for treatment of heart failure (HF), but the intra-individual biological variation is high. We investigated whether changes in sodium intake and posture contribute to this variation.

Methods and results: A total of 12 healthy individuals and 12 patients with medically treated compensated HF were examined after 1 week of low (70 mmol [1.61 g] per day) and 1 week of high (250 mmol [5.75 g] per day) sodium intake. Plasma volume and plasma concentrations of BNP and proBNP were determined after 1 h in seated and 1 h in supine position. In healthy individuals, the plasma BNP concentration increased significantly on high sodium intake with a ratio (high sodium/low sodium) of 2.00 (1.32–3.03, P = 0.004). The corresponding values for HF patients were 1.69 (1.25–2.29, P = 0.003). The plasma BNP concentration changed modestly by a posture change, with a plasma BNP ratio (supine/seated) of 1.15 (1.07–1.14, P = 0.001) and 1.06 (0.99–1.24, P = 0.088) in healthy subjects and HF patients, respectively. Plasma proBNP concentrations were neither significantly affected by posture nor by sodium intake.

Conclusion: Sodium intake has a considerable effect on plasma BNP and therefore contributes to the intra-individual variability. We suggest dietary sodium intake to be standardized at least 3 days prior to blood sampling for the determination of plasma BNP.

Key Words: Plasma volume • Posture • Variability


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Conclusion
 Funding
 Acknowledgements
 Reference
 
B-type natriuretic peptide (BNP) is predominantly secreted from the atria of the normal heart and from the ventricles of the failing heart in response to wall stress.1 During the past decade, plasma BNP concentrations have been established to be a valuable tool in the diagnosis of heart failure (HF),2 and it has recently been suggested that medical therapy in symptomatic HF patients can be adjusted according to individual changes in plasma BNP.3 The intra-individual variation of plasma BNP and proBNP concentrations, however, is considerable even during stable steady-state clinical conditions.4–6 The minimal percental change in serial measurements that represents a true change in plasma BNP (i.e. the reference change value, RCV) has been reported to vary between 113 (week to week) and 169% (8 weeks).4,5

To reduce the intra-individual variation, it is important to identify the factors that might affect plasma BNP and proBNP concentrations such as sodium intake before blood sampling and the body posture during blood sampling. These factors are major determinants of the central intravascular volume and might therefore be expected to affect the release of BNP. Conflicting results have been reported concerning the impact of posture shifts as well as the effect of altered sodium intake on plasma BNP concentrations in healthy individuals7–10 and in HF patients.8,11–13

In earlier studies, however, the participants were investigated with respect to either posture or alterations in sodium intake without controlling for a possible interaction. On the basis of a recent publication,14 we therefore examined the effect of 1 week of a low and 1 week of a high sodium intake, in seated and supine healthy individuals and compensated HF patients on plasma BNP and proBNP concentrations.


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 Conclusion
 Funding
 Acknowledgements
 Reference
 
The experimental protocol was approved by the Ethics Committee of Copenhagen (KF 01-063/02) and was in agreement with the institutional guidelines and principles in the declaration of Helsinki. Written informed consent was obtained from all subjects. The experimental protocol has been described in detail previously.14

Subjects
Fifteen male patients with compensated HF were recruited from three outpatients clinics at Copenhagen University Hospital (Bispebjerg Hospital, Frederiksberg Hospital and Rigshospitalet). Fourteen age-matched healthy control subjects were recruited through public advertisement. Three patients and two healthy individuals were excluded due lack of compliance to the diet or due to vasovagal episodes. Baseline characteristics of the HF patients (New York Heart Association (NYHA) functional class II, n = 6; NYHA class III, n = 6) and healthy individuals completing the study are presented in Table 1.


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  		Table 1 Baseline data

 
All healthy individuals exhibited a normal medical history and normal values of clinical evaluations, supine blood pressure (<140/85), urine dipstick test, spirometry, and echocardiography.

The HF diagnosis (ischaemic, n = 8 and idiopathic, n = 4) was based on clinical and radiological evaluation in combination with evidence of impaired left ventricular ejection fraction (LVEF) of <40%. None of the patients had a recent history of acute myocardial infarction, angina pectoris, or cardiac decompensation (<2 months). The patients received ACE inhibitors (n = 11), angiotensin receptor blockers (n = 1), {alpha}/ß-adrenoreceptor blockers (n = 5), ß-adrenoreceptor blockers (n = 7), diuretics (n = 10), spironolactone (n = 4), digoxin (n = 1), long-acting nitrates (n = 2), statines (n = 10) and low-dose aspirin (n = 10). The pharmacological treatment was kept unchanged for 2 weeks prior to the study.

Experimental protocol
The study consisted of two consecutive 7-day periods, where all participants shifted between a diet with a daily content of 70 mmol sodium (1.61 g) and 250 mmol sodium (5.75 g) or vice versa in a balanced randomized fashion. The variation in sodium content reflects the normal range of sodium intake in western countries.15 Water intake was ad libitum. Adherence to the diet was demonstrated by 24-h urine collections for at least 3 days before the examinations. The participants were examined in the final day of each dietary sodium level (day 7) after overnight fasting and were instrumented with short peripheral catheters in anticubital veins for blood sampling while resting in an armchair. Blood samples were collected in vacutainers containing Na2–EDTA (1.5 mg/mL) following 1 h of seated and 1 h of supine rest. The samples were immediately centrifuged at 3700 rpm for 10 min, and the plasma was stored in a –80°C freezer for later analysis.

The techniques for measurements of plasma volume and urine sodium concentration have been described in detail previously.14

BNP and proBNP analyses
The BNP concentrations in plasma were measured in duplicates with a commercial assay (Bayer, ADVIA Centaur). This assay detects BNP-32 with no cross-reactivity to proBNP.16 Lowest level of detection is 0.14 pmol/L (1 pmol/L equals 3.46 pg/mL). The within-runs assay imprecision is 4.3% at 8.5 pmol/L and 1.8% at 119 pmol/L according to the manufacturer.

The total proBNP concentration in plasma was measured in duplicates with a processing independent assay.17 This assay quantifies the total concentration of prohormone products after a pre-analytical enzymatic step. Briefly, plasma is mixed with a protease (trypsin) that cleaves proBNP after an amino acid in position 21. In this way, intact proBNP and its N-terminal fragment are both cleaved into the same analyte. The released fragment is measured with a conventional radioimmunoassay specific for the N-terminal decapeptide. Assay imprecision within-runs are 12% at 13 pmol/L and 5% at 130 pmol/L, and the assay sensitivity is 0.2 pmol/L. Measurement with this assay compares well with the NT-proBNP assay from Roche in patients with stable HF with a factor of 1.14 difference (r = 0.93, P < 0.001, J. P. Goetze, unpublished results).

Data presentation and statistics
The data regarding renal sodium excretion, mean plasma volume, and mean proBNP concentrations have been published recently.14 The data were tested for normality in distribution within each group (Healthy and HF) in each posture (seat and supine) by visual inspection and the Kolmogorov–Smirnoff test. BNP was normal distributed after log transformation, whereas ProBNP could not be transformed to normality in all subgroups. Treatment effects ({Delta}log BNP, {Delta}log proBNP, and {Delta}PV) of sodium and posture were normally distributed after log transformation. Plasma concentrations of proBNP below detection limits were set to 0.2 pmol/L (detection limit).

According to the crossover design of the study, a period effect was ruled out for each group separately (Healthy and HF) by comparing the treatment (sodium) response in subjects changing from low to high sodium with the subjects changing from high to low (unpaired t-test or Mann–Whitney U-test). Thereafter, a possible period vs. treatment interaction (carry-over effect) was ruled out in each group separately (Healthy and HF) by comparing the mean response to low and high sodium in the subjects receiving low–high and high–low sodium (unpaired t-test or Mann–Whitney U-test). Subsequently, the data could be pooled for each group (Healthy and HF) in a low- and a high sodium group regardless of which order the treatments were given.

Differences in baseline variables (Table 1) between the groups (Healthy vs. HF) were tested by paired t-tests. The effect of sodium and posture on log proBNP and log BNP concentrations were analysed in each group separately (Healthy and HF) by a multivariate regression model with sodium, posture, and sodium vs. posture as fixed effects using an unstructured covariance matrix for the four repeated measures per subject. Excluding a sodium vs. posture interaction, the model was subsequently reduced to include sodium and posture as fixed effects. The effect of time (days) on renal sodium excretion within the groups (Healthy and HF) on final 3 days of high and low sodium intake was analysed by the same model using a compound symmetry covariance matrix for the three repeated measures per subject.

Baseline data are presented as means ± SD. Urinary sodium excretion is stated as means with 95% CI. The effects of posture and sodium are stated as geometric mean ratios with 95% CI except if not otherwise stated. The statistical analyses were performed using the SAS System for Windows V9.1 (SAS Institute Inc., Cary, NC, USA). All statistical tests were two-sided with a significance level of 0.05.


   Results
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 Abstract
 Introduction
 Methods
 Results
Discussion
 Conclusion
 Funding
 Acknowledgements
 Reference
 
Sodium intake and renal excretion
Steady-state conditions between sodium intake and renal sodium output were obtained during the final 3 days at each level of sodium intake. The renal sodium output of the healthy individuals were 208 ± 33, 216 ± 27, and 203 ± 28 mmol/day during the final 3 days of the high sodium intake (no significant difference, P = 0.488), and 61 ± 13, 57 ± 14, and 53 ± 8 mmol/day during the final 3 days of the low (no significant difference, P = 0.374). The corresponding values for HF patients were 218 ± 31, 209 ± 25, and 201 ± 17 mmol/day (no significant difference, P = 0.217) and 67 ± 15, 64 ± 15, and 60 ± 16 mmol/day (no significant difference, P = 0.664).

Plasma volume
The individual responses to altered sodium intake and posture shifts are shown in Figure 1. Apart from one healthy subject and one HF patient, all participants exhibited plasma volume expansion during the high sodium intake. A posture change from seated to supine increased plasma volume in all of the participants.


Figure 1
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  		Figure 1 Plasma volume during (A) low and high sodium intake and (B) in seated and in supine position. Open circles represent healthy subjects (n = 11, high sodium supine); closed squares refer to HF (n = 11, high sodium seat); open and closed triangles refer to mean values.

 
Plasma concentrations of BNP and proBNP
There was no significant interaction between sodium intake and posture on plasma BNP concentrations neither in healthy individuals (P = 0.460) nor in HF patients (P = 0.159).

In healthy individuals, the plasma BNP concentration increased significantly on high sodium intake with a ratio (high /low sodium) of 2.00 (1.32–3.03, P = 0.004). The corresponding values for HF patients were 1.69 (1.25–2.29, P = 0.003). Notably, in all but one healthy subject, BNP increased during high sodium intake (Figure 2). The plasma BNP concentration changed modestly by a posture change, with a plasma BNP ratio (supine/seated) of 1.15 (1.07–1.24, P = 0.001) and 1.06 (0.99–1.14, P = 0.088) in healthy subjects and HF patients, respectively.


Figure 2
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  		Figure 2 B-type natriuretic peptide during (A) low and high sodium intake and (B) in seated and supine position. Open circles refer to healthy subjects; closed squares refer to HF; open and closed triangles refer to geometric mean values; dotted line refers to limit of detection.

 
There was no significant interaction between sodium intake and posture on plasma proBNP concentrations neither in healthy individuals (P = 0.363) nor in HF patients (P = 0.253). In healthy individuals and HF patients, the plasma proBNP concentration ratio (high/low sodium) was 1.52 (0.47–4.99; P = 0.450) and 1.47 (0.84–2.56, P = 0.157). Likewise no effect was observed during a posture change where the plasma BNP ratios (supine/seated) were 0.96 (0.53–1.73, P = 0.869) in healthy individuals and 0.93 (0.51–1.73, P = 0.811) in HF patients (Figure 3).


Figure 3
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  		Figure 3 Pro-B-type natriuretic peptide during (A) low and high sodium intake and (B) in seated and in supine position. Open circles refer to healthy subjects; closed squares refer to HF; open and closed triangles refer to medians; dotted line refers to limit of detection.

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Conclusion
 Funding
 Acknowledgements
 Reference
 
The main finding of the present study is that plasma BNP, but not plasma proBNP concentrations, vary significantly by changes in dietary sodium intake. In contrast, a posture shift (seated to supine) affects plasma BNP only modestly, whereas proBNP concentrations still remain unaltered. The responses are similar in healthy individuals and in HF patients.

BNP and sodium intake
In a recent study of cardiovascular and neuroendocrine responses to changes in dietary sodium intake, we reported that the mean plasma proBNP concentration surprisingly remained unchanged despite a considerable intravascular central volume expansion induced by 1-week of high sodium intake.14 Owing to this unexpected finding, we decided to extend the analysis by measuring the plasma BNP concentrations in all participants in order to evaluate whether the bioactive hormone reflects acute and subacute volume changes better than the precursor. In this investigation, we therefore present the individual responses of plasma volume, proBNP, and BNP to variations in sodium intake (Figures 1Go3). We found that in contrast to the precursor, plasma BNP increased significantly in response to the moderate physiological increase in sodium intake, probably because of the central blood volume expansion. Notably, the effect of sodium intake was similar in both postures.

In previous investigations, plasma BNP concentrations have been less affected than we observed despite more extreme variations in sodium intake. Wambach et al.10 increased sodium intake from 40 to 300 mmol/day (0.92–6.90 g/day) and reported no changes in plasma BNP levels. Lang et al.9 modulated dietary sodium intake from 171 to 503 mmol/day (3.93–11.56 g/day), which increased the mean BNP concentration from 1.33 to 2.04 pmol/L. In patients with mild to moderate hypertension, Buckley et al.18 varied the sodium intake from 10 to 350 mmol/day (0.23–8.05 g/day), which increased the mean plasma BNP concentrations from ~4 to 9 pg/mL. Although different postures (upright and semirecumbent, supine) were used in the studies, our results indicate that this cannot explain the conflicting results. However, other differences between the protocols such as duration of the diets (5 or 7 days) and washout periods in-between diets might also have contributed to these discrepancies. In addition, it is possible that the osmotic active accumulation of sodium and water19 and thereby release of BNP is attenuated at extreme high sodium intakes. Furthermore, the potential lack of control of other confounding factors such as exercise and circadian rhythms, which are known to affect plasma BNP levels,4,20,21 might also explain the discrepant results of the different studies. Finally, the development of new and more sensitive methods to measure plasma BNP without cross-reactivity to the related atrial natriuretic peptide might have improved the ability to detect the minor effects even at very low molar concentrations.1

The HF patients exhibited similar relative responses to alterations in sodium intake as healthy individuals. In previous studies, BNP concentrations were suppressed during sodium restriction in medically treated patients with congestive HF,12 whereas the BNP levels remained unchanged despite sodium loading in asymptomatic untreated HF patients.13 Treatment with ACE inhibitors,22 ß-adrenoreceptor blockers,23 and spironolactone24 has been shown to reduce plasma levels of BNP, and it is possible that the release of BNP in response to sodium loading is normalized during medical treatment.

BNP and posture
Despite a considerable plasma volume expansion induced by the shift from seated to supine position, plasma BNP increased only modestly in both groups (Healthy and HF). The response probably reflects the cellular mechanism of release, i.e. constitutive secretion, which does not allow the plasma concentrations to vary much during short-term interventions. Accordingly, during a posture shift from seated to supine, plasma BNP concentrations have been reported to decrease,8 increase,7 or remain unchanged11 in healthy individuals7,8 and in patients with congestive HF.8,11 Our findings suggest, however, that the modest effect of posture might be masked, if effects of other factors such as sodium intake, exercise,20,21 and circadian rhythms4 are not taken into consideration. Not all of these factors have been strictly controlled previously,8,11 which might explain the divergent results.

BNP vs. proBNP during posture shifts and changes in sodium intake
In contrast to BNP, plasma proBNP concentrations remained unaffected by changes in sodium intake and posture (Figure 3). It is well known that the plasma concentrations of proBNP is higher per se, whereas the half life is considerably longer.25,26 As a consequence, proBNP may exhibit more stable circulatory plasma levels than BNP, which could explain the lower sensibility to acute (posture shifts) and subacute (sodium loading) changes in central blood volume. Accordingly, the biological variation and the RCV have been reported to be lower for proBNP than for BNP by some authors,5 but not by all.4 It is conceivable, however, that proBNP would increase during sustained central intravascular volume expansion as induced by prolonged high sodium intake. Furthermore, it is reasonable to argue that the present results could be explained by the use of different assays for measuring BNP and proBNP in plasma. However, although some differences in molar concentrations must be expected because of different calibrators, the currently available BNP assays all measure the bioactive peptide with antibodies directed against epitopes within the C-terminal ring structure of BNP-321. The NT-proBNP assay from Roche most likely measures the N-terminal fragment 1–76 as well as the intact proBNP although with a lower affinity for the latter (J. P. Goetze, unpublished results). We have compared the NT-proBNP assay against the present proBNP radioimmunoassay, and generally they compare well. In an earlier study, NT-proBNP measurements also compared well to plasma concentrations obtained with a non-commercial proBNP radioimmunoassay with a systematic difference between high and low concentrations.27 Notably, the average difference between the two assays reported by Throughton et al.27 is almost exactly the same as for the presently used PIA proBNP assay to the Roche NT-proBNP assay (factor 1.3 vs.1.4). We therefore believe that our findings would also be reflected using other methodologies including the NT-proBNP assay.


   Conclusion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusion
Funding
 Acknowledgements
 Reference
 
In healthy individuals and patients with medically treated and compensated HF, plasma BNP concentrations were two-fold higher during the high vs. the low sodium intake. A posture shift from seated to supine increased plasma BNP modestly. ProBNP concentrations remained unchanged irrespective of sodium intake and posture. Thus, whereas the contribution of posture to the intra-individual variability in plasma BNP can be considered negligible, the effect of variations in sodium intake must be taken into account. We suggest that sodium intake should be standardized for at least 3 days before sampling of blood for determination of plasma BNP.


   Funding
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusion
 Funding
Acknowledgements
 Reference
 
Danish Research Councils (2006-01-0012). Danish Heart Foundation (02-1-3-40-22986).


   Acknowledgements
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusion
 Funding
 Acknowledgements
Reference
 
We gratefully acknowledge the skilful technical assistance of Lone Olsen. Bayer Diagnostics, Denmark, kindly provided the BNP analyses.

Conflict of interest: none declared.


   Reference
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusion
 Funding
 Acknowledgements
 Reference
 

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