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Consumo de sal como

factor de riesgo para


Article: Anlisis de la evidencia experimental que muestra efectos nocivos de

la sal y su relacin con la hipertensin arterial
Ignacio BravoLuis / MicheaMedwave 01/2012

The study by Taylor et al published in June 2010 in the American Journal of
Hypertension questions the effectiveness of reducing salt intake in the diet in the
prevention and treatment of high blood pressure and other cardiovascular
conditions. The publication of this article has lead to great controversy and medical
associations and learned societies responded promptly. The response criticized the
results of the meta-analysis and pointed out its methodological shortcomings. In this
review we critically appraise the experimental evidence that shows the importance
of diet salt intake and its role as a determinant of blood pressure. We briefly
describe the paradigm that explains the role of salt intake in contributing in the
regulation of blood pressure (Guyton hypothesis and model) and we mention the
experimental evidence that supports this. We briefly comment on the classical
studies that indicate that salt intake (NaCl) contributes directly to the development
of high blood pressure and target tissues. Finally, we briefly mention the
experimental data that is related with the controversy on the role of salt (NaCl) or
sodium as prohypertensive agents.

The Significance of Duration and Amount of Sodium Reduction Intervention in Normotensive and
Hypertensive Individuals: A Meta-Analysis.
Graudal N, Hubeck-Graudal T, Jrgens G, McCarron DA.

The purpose of this meta-analysis was to establish the time for achievement of maximal blood pressure (BP)
efficacy of a sodium reduction (SR) intervention and the relation between the amount of SR and the BP response in
individuals with hypertension and normal BP. Relevant studies were retrieved from a pool of 167 randomized
controlled trials (RCTs) published in the period 1973-2010 and integrated in meta-analyses. Fifteen relevant RCTs
were included in the maximal efficacy analysis. After initiation of sodium reduction (range: 55-118 mmol/d), there
were no significant differences in systolic blood pressure (SBP) or diastolic blood pressure (DBP) between
measurements at weeks 1 and 2 (SBP: -0.18 mmHg/DBP: 0.12 mmHg), weeks 1 and 4 (SBP: -0.50 mmHg/DBP:
0.35 mmHg), weeks 2 and 4 (SBP: -0.20 mmHg/DBP: -0.10 mmHg), weeks 2 and 6 (SBP: -0.50 mmHg/DBP:
-0.42 mmHg), and weeks 4 and 6 (SBP: 0.39 mmHg/DBP: -0.22 mmHg). Eight relevant RCTs were included in the
dose-response analysis, which showed that within the established usual range of sodium intake [<248 mmol/d
(5700 mg/d)], there was no relation between the amount of SR (range: 136-188 mmol) and BP outcome in
normotensive populations [SBP: 0.99 mm Hg (95% CI: 2.12, 4.10), P = 0.53; DBP: -0.49 mm Hg (95% CI: -4.0,
3.03), P = 0.79]. In contrast, prehypertensive and hypertensive populations showed a significant dose-response
relation (range of sodium reduction: 77-140 mmol/d) [SBP: 6.87 mmHg (95% CI: 5.61, 8.12, P < 0.00001); DBP:
3.61 mmHg (95% CI: 2.83, 4.39, P < 0.00001)]. Consequently, the importance of kinetic and dynamic properties of
sodium reduction, as well as baseline BP, should probably be considered when establishing a policy of sodium

2015 American Society for Nutrition.

KEYWORDS: blood pressure; dietary guidelines; meta-analysis; pharmacodynamics; pharmacokinetics; salt;


High salt intake increases blood pressure via BDNF-mediated down regulation
of KCC2 and impaired baroreflex inhibition of vasopressin neurons.
Choe KY, Han SY, Gaub P, Shell B, Voisin DL, Knapp BA, Barker PA, Brown CH,
Cunningham JT, Bourque CW.

The mechanisms by which dietary salt promotes hypertension are unknown. Previous
work established that plasma [Na(+)] and osmolality rise in proportion with salt intake
and thus promote release of vasopressin (VP) from the neurohypophysis. Although
high levels of circulating VP can increase blood pressure, this effect is normally
prevented by a potent GABAergic inhibition of VP neurons by aortic baroreceptors.
Here we show that chronic high salt intake impairs baroreceptor inhibition of rat VP
neurons through a brain-derived neurotrophic factor (BDNF)-dependent activation of
TrkB receptors and downregulation of KCC2 expression, which prevents inhibitory
GABAergic signaling. We show that high salt intake increases the spontaneous firing
rate of VP neurons in vivo and that circulating VP contributes significantly to the
elevation of arterial pressure under these conditions. These results provide the first
demonstration that dietary salt can affect blood pressure through neurotrophininduced plasticity in a central homeostatic circuit.

A mathematical model of salt-sensitive hypertension: the neurogenic hypothesis.

Averina VA, Othmer HG, Fink GD, Osborn JW.

Salt sensitivity of arterial pressure (salt-sensitive hypertension) is a serious global health issue. The
causes of salt-sensitive hypertension are extremely complex and mathematical models can elucidate
potential mechanisms that are experimentally inaccessible. Until recently, the only mathematical model
for long-term control of arterial pressure was the model of Guyton and Coleman; referred to as the G-C
model. The core of this model is the assumption that sodium excretion is driven by renal perfusion
pressure, the so-called 'renal function curve'. Thus, the G-C model dictates that all forms of hypertension
are due to a primary shift of the renal function curve to a higher operating pressure. However, several
recent experimental studies in a model of hypertension produced by the combination of a high salt intake
and administration of angiotensin II, the AngII-salt model, are inconsistent with the G-C model. We
developed a new mathematical model that does not limit the cause of salt-sensitive hypertension solely
to primary renal dysfunction. The model is the first known mathematical counterexample to the
assumption that all salt-sensitive forms of hypertension require a primary shift of renal function: we
show that in at least one salt-sensitive form of hypertension the requirement is not necessary. We will
refer to this computational model as the 'neurogenic model'. In this Symposium Review we discuss how,
despite fundamental differences between the G-C model and the neurogenic model regarding
mechanisms regulating sodium excretion and vascular resistance, they generate similar haemodynamic
profiles of AngII-salt hypertension. In addition, the steady-state relationships between arterial pressure
and sodium excretion, a correlation that is often erroneously presented as the 'renal function curve', are
also similar in both models. Our findings suggest that salt-sensitive hypertension is not due solely to renal
dysfunction, as predicted by the G-C model, but may also result from neurogenic dysfunction.

Salt intake in children and its consequences on blood pressure.

Lava SA, Bianchetti MG, Simonetti GD.

Sodium is the most abundant extracellular cation and therefore pivotal in
determining fluid balance. At the beginning of life, a positive sodium balance is
needed to grow. Newborns and preterm infants tend to lose sodium via their kidneys
and therefore need adequate sodium intake. Among older children and adults,
however, excessive salt intake leads to volume expansion and arterial hypertension.
Children who are overweight, born preterm, or small for gestational age and African
American children are at increased risk of developing high blood pressure due to a
high salt intake because they are more likely to be salt sensitive. In the developed
world, salt intake is generally above the recommended intake also among children.
Although a positive sodium balance is needed for growth during the first year of life,
in older children, a sodium-poor diet seems to have the same cardiovascular
protective effects as among adults. This is relevant, since: (1) a blood pressure
tracking phenomenon was recognized; (2) the development of taste preferences is
important during childhood; and (3) salt intake is often associated with the
consumption of sugar-sweetened beverages (predisposing children to weight gain).

Dietary salt intake and hypertension.

Ha SK1.

Over the past century, salt has been the subject of intense scientific research related to blood pressure
elevation and cardiovascular mortalities. Moderate reduction of dietary salt intake is generally an effective
measure to reduce blood pressure. However, recently some in the academic society and lay media dispute
the benefits of salt restriction, pointing to inconsistent outcomes noted in some observational studies. A
reduction in dietary salt from the current intake of 9-12 g/day to the recommended level of less than 5-6
g/day will have major beneficial effects on cardiovascular health along with major healthcare cost savings
around the world. The World Health Organization (WHO) strongly recommended to reduce dietary salt
intake as one of the top priority actions to tackle the global non-communicable disease crisis and has urged
member nations to take action to reduce population wide dietary salt intake to decrease the number of
deaths from hypertension, cardiovascular disease and stroke. However, some scientists still advocate the
possibility of increased risk of CVD morbidity and mortality at extremes of low salt intake. Future research
may inform the optimal sodium reduction strategies and intake targets for general populations. Until then,
we have to continue to build consensus around the greatest benefits of salt reduction for CVD prevention,
and dietary salt intake reduction strategies must remain at the top of the public health agenda.