Cardiovascular Journal of Africa: Vol 29 No 3 (May/Junel 2018)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 29, No 3, May/June 2018 AFRICA 175
other hand, the significantly higher BMI and higher proportion
of overweight/obese women resulted in the masking of the
relationship in the female group. Since women made up 63% of
the total population sample, the masking effects of this female
group are imputed to the whole population sample.
Mechanisms responsible for the masking effects seem to be
mediated by leptin. Plasma renin and insulin levels were similar
between the different groups but leptin was significantly higher
in the overweight/obese group, especially in women. This could
account for the significantly lower urinary sodium excretion rate
in the overweight/obese women compared to normal-weight
women. As explained earlier, women made up 63% of this
population and 75% of them were overweight or obese, therefore
they were responsible for the significantly lower urinary sodium
excretion rate (106 mmol/day) in this population compared to
other population groups.
In a study conducted in 45 countries with a total of 69 011
participants, the average 24-hour urinary sodium excretion rate
was 159.4 mmol/day.35 In a Chinese study, the average 24-hour
urinary sodium excretion was 235 mmol/day,3 which is more than
double that of our population. A low sodium excretion rate of
104 mmol/day was observed in the trials of the Hypertension
Prevention Collaborative Research Group.36 However in this study,
the participants were on a low-sodium diet. The relatively low
urinary sodium excretion rate is unique to our population sample
and it may account for the leptin-mediated masking effects.
The significantly higher leptin concentrations in the
overweight/obese groups, especially in women where it was more
than three times higher than that of the overweight/obese males,
mediated the masking effects. Normally sodium intake results in
a slight increase in BP due to volume expansion. This causes an
increased sodium excretion rate through pressure natriuresis. A
steady state is reached where sodium intake is equal to sodium
excretion. However in the presence of high leptin concentrations
the steady state is not achieved.
Although leptin stimulates the sympathetic nervous system, it
also increases nitric oxide concentration.37 Therefore, the pressor
effects of the sympathetic nervous system are counteracted by
the depressor effects of nitric oxide. Consequently there is no net
change in BP. Without an increase in BP, pressure natriuresis is
suppressed, resulting in a reduced urinary sodium excretion rate.
This explains the significantly lower urinary sodium excretion
rates in overweight/obese women and in the total population
sample since women constituted 63% of this sample.
The low urinary sodium concentration leads to a narrow
range of urinary sodium concentration. As a consequence,
the relationship between 24-hour urinary sodium excretion
and BP is blunted. The masking of a relationship due to low
concentrations is called a regression dilution.3 To the best of
our knowledge, this is the first study to show that increased
BMI masks the relationship between 24-hour urinary sodium
excretion and BP, and that leptin mediates the mechanisms
responsible for the masking effect.
Potential limitations of our study are as follows; firstly,
we collected once-off 24-hour urine samples and this does
not account for the daily variation in dietary sodium intake.
Although 24-hour urinary sodium excretion is an acceptable
index of dietary sodium intake, the once-off 24-hour urine
sample does not take into account the within- and between-
person sodium intake variations. Secondly, the covariates
such as alcohol intake and smoking were obtained through a
self-reported questionnaire and therefore may not have been
accurate. Thirdly, we did not use a dietary recall questionnaire
to assess sodium intake. This could have been a useful tool for
assessing the accuracy of 24-hour urinary sodium excretion as an
index of dietary sodium intake. Finally, this was a cross-sectional
study, therefore conclusions regarding cause and effect must be
drawn with caution.
Conclusion
This study indicates that dietary sodium intake influenced BP
in this population, however this relationship could only be
observed in lean participants, since increased BMI masked this
relationship. These data suggest that future studies must take
into account the high prevalence of obesity in this population
before any conclusions are drawn on the relationship between
sodium intake and BP.
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