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Hemodynamic and Autonomic Response to Different Salt Intakes in Normotensive Individuals

View Article: PubMed Central - PubMed

ABSTRACT

Background: Even if sodium sensitivity represents a risk factor at any blood pressure (BP) level, limited evidence is available that it may influence cardiovascular control in normotensives, particularly in white individuals. Therefore, the aim of the study was to investigate whether sodium sensitivity alters hemodynamic or autonomic responses to salt in normotensives.

Methods and results: We evaluated the Sodium‐Sensitivity Index (SS‐Index) in 71 white normotensives after 5 days of high‐ and low‐sodium diets. We measured BP continuously at the end of each period, estimating hemodynamic indices from BP waveform analysis, and autonomic indices from heart rate (HR) and BP variability. According to the SS‐Index distribution, we defined 1 sodium‐sensitive group (SS, with SS‐Index >15 mm Hg/[mmol·day]), 1 sodium‐resistant group, (unresponsive to sodium load with −15≤ SS‐Index ≤+15), and 1 inverse sodium‐sensitive group, responsive to sodium by decreasing BP, with SS‐Index <−15). We compared the effects of the diets among groups, and correlated autonomic/hemodynamic indices with the SS‐Index. After sodium loading, a significant decrease in systemic peripheral resistances, HR, spectral indices of BP modulation, and a significant increase of indices of HR vagal modulation were found in the inverse sodium‐sensitive group but not in SS normotensives. Moreover, the highest SS‐Indices were associated with the lesser vagal HR decelerations.

Conclusions: Our data suggest that salt sensitivity in white normotensive individuals is associated with impaired vasodilation and altered autonomic response to dietary salt. Such dysfunction may critically contribute to induce a BP response to dietary salt.

No MeSH data available.


Autonomic indices of HR variability. Left: frequency‐ and complexity‐domain indices of cardiac sympatho/vagal balance (PI LF/HF and α1); right: frequency‐ and time‐domain indices of vagal modulations of HR (PI HF and NN50+), in inverse sodium‐sensitive (ISS), sodium‐resistant (SR), and sodium‐sensitive (SS) individuals. α1 indicates short‐term scale coefficient of PI; HF indicates high frequency; HR, heart rate; LF, low frequency; NN50+, number of PI increases per minute larger than 50 ms; PI, pulse interval. Spectral indices are represented in logarithmic scale. The “*” marks significant differences between diets.
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jah31673-fig-0003: Autonomic indices of HR variability. Left: frequency‐ and complexity‐domain indices of cardiac sympatho/vagal balance (PI LF/HF and α1); right: frequency‐ and time‐domain indices of vagal modulations of HR (PI HF and NN50+), in inverse sodium‐sensitive (ISS), sodium‐resistant (SR), and sodium‐sensitive (SS) individuals. α1 indicates short‐term scale coefficient of PI; HF indicates high frequency; HR, heart rate; LF, low frequency; NN50+, number of PI increases per minute larger than 50 ms; PI, pulse interval. Spectral indices are represented in logarithmic scale. The “*” marks significant differences between diets.

Mentions: Considering HR variability (Figure 3), the high‐salt diet decreased spectral and complexity‐based indices of cardiac sympatho/vagal balance (PI LF/HF decreased by −21%, −20%, and −16% and α1 decreased by −6%, −4%, and −7% in ISS, SR, and SS groups, respectively). The high‐salt diet also increased time‐domain and spectral indices of vagal HR modulation (+32%, +36%, and +24% for NN50+, +51%, +54%, and +38% for PI HF, in ISS, SR, and SS groups, respectively). The vagal HR modulation tended to decrease with the severity of sodium sensitivity and the effect of sodium loading appeared less marked in the SS group.


Hemodynamic and Autonomic Response to Different Salt Intakes in Normotensive Individuals
Autonomic indices of HR variability. Left: frequency‐ and complexity‐domain indices of cardiac sympatho/vagal balance (PI LF/HF and α1); right: frequency‐ and time‐domain indices of vagal modulations of HR (PI HF and NN50+), in inverse sodium‐sensitive (ISS), sodium‐resistant (SR), and sodium‐sensitive (SS) individuals. α1 indicates short‐term scale coefficient of PI; HF indicates high frequency; HR, heart rate; LF, low frequency; NN50+, number of PI increases per minute larger than 50 ms; PI, pulse interval. Spectral indices are represented in logarithmic scale. The “*” marks significant differences between diets.
© Copyright Policy - creativeCommonsBy-nc
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5015293&req=5

jah31673-fig-0003: Autonomic indices of HR variability. Left: frequency‐ and complexity‐domain indices of cardiac sympatho/vagal balance (PI LF/HF and α1); right: frequency‐ and time‐domain indices of vagal modulations of HR (PI HF and NN50+), in inverse sodium‐sensitive (ISS), sodium‐resistant (SR), and sodium‐sensitive (SS) individuals. α1 indicates short‐term scale coefficient of PI; HF indicates high frequency; HR, heart rate; LF, low frequency; NN50+, number of PI increases per minute larger than 50 ms; PI, pulse interval. Spectral indices are represented in logarithmic scale. The “*” marks significant differences between diets.
Mentions: Considering HR variability (Figure 3), the high‐salt diet decreased spectral and complexity‐based indices of cardiac sympatho/vagal balance (PI LF/HF decreased by −21%, −20%, and −16% and α1 decreased by −6%, −4%, and −7% in ISS, SR, and SS groups, respectively). The high‐salt diet also increased time‐domain and spectral indices of vagal HR modulation (+32%, +36%, and +24% for NN50+, +51%, +54%, and +38% for PI HF, in ISS, SR, and SS groups, respectively). The vagal HR modulation tended to decrease with the severity of sodium sensitivity and the effect of sodium loading appeared less marked in the SS group.

View Article: PubMed Central - PubMed

ABSTRACT

Background: Even if sodium sensitivity represents a risk factor at any blood pressure (BP) level, limited evidence is available that it may influence cardiovascular control in normotensives, particularly in white individuals. Therefore, the aim of the study was to investigate whether sodium sensitivity alters hemodynamic or autonomic responses to salt in normotensives.

Methods and results: We evaluated the Sodium‐Sensitivity Index (SS‐Index) in 71 white normotensives after 5 days of high‐ and low‐sodium diets. We measured BP continuously at the end of each period, estimating hemodynamic indices from BP waveform analysis, and autonomic indices from heart rate (HR) and BP variability. According to the SS‐Index distribution, we defined 1 sodium‐sensitive group (SS, with SS‐Index >15 mm Hg/[mmol·day]), 1 sodium‐resistant group, (unresponsive to sodium load with −15≤ SS‐Index ≤+15), and 1 inverse sodium‐sensitive group, responsive to sodium by decreasing BP, with SS‐Index <−15). We compared the effects of the diets among groups, and correlated autonomic/hemodynamic indices with the SS‐Index. After sodium loading, a significant decrease in systemic peripheral resistances, HR, spectral indices of BP modulation, and a significant increase of indices of HR vagal modulation were found in the inverse sodium‐sensitive group but not in SS normotensives. Moreover, the highest SS‐Indices were associated with the lesser vagal HR decelerations.

Conclusions: Our data suggest that salt sensitivity in white normotensive individuals is associated with impaired vasodilation and altered autonomic response to dietary salt. Such dysfunction may critically contribute to induce a BP response to dietary salt.

No MeSH data available.