Restricting salt intake reverses vascular endothelial dysfunction in people with moderately increased blood pressure (BP), shows a randomized study published in the Journal of the American College of Cardiology.
The effects were independent of changes in the participants' systolic BP, leading the researchers to suggest that salt causes vascular dysfunction beyond its effect on BP.
Editorialists David Celermajer (Royal Prince Alfred Hospital, Sydney, Australia) and Bruce Neal (Sydney Medical School) sound a note of caution, however, saying that simply controlling for BP is unreliable because of "enormous moment-to-moment within-individual variability" of BP.
But they say that the study is a reminder that "a simple molecule such as sodium can assault our vessels in complex maladaptive ways," adding: "Our next challenge is to translate this knowledge derived from vascular biology into effective and appropriate public health strategy."
The study had a crossover design. The 17 participants reduced their dietary sodium intake to a target of about 50 mmol/day, verified by urinary excretion and dietary analysis. For one 5-week period, the participants took a daily slow-release sodium chloride tablet that brought their salt intake up to about 150 mmol/day. For the other 5-week period of the study they took a placebo tablet.
Salt restriction had notable effects on both macrovascular and microvascular function, report study author Douglas Seals (University of Colorado at Boulder, USA) and team.
Flow-mediated dilation of the brachial artery was 68% greater during restricted than usual salt intake, at 6.01% versus 3.57%. Flow-mediated dilatation increased during restricted salt intake in all but two participants.
There were similar benefits for the microcirculation, with forearm blood flow increased by 42% in response to intrabrachial artery infusion of acetylcholine during salt restriction and BP-corrected forearm vascular conductance increased by 52%. Again, the effects were seen in all but two participants.
The team found that the endothelial benefits of salt restriction were mediated by increased bioavailability of nitric oxide and tetrahydrobiopterin, and by reduced oxidative stress; infusion of antioxidants improved endothelial function during normal but not restricted salt intake.
As anticipated, systolic BP was significantly lower during restricted- versus usual-salt intake, at an average of 128 versus 140 mmHg.
Celermajer and Neal note that "normal" salt intake as defined by current standards is far higher than what was consumed for most of human evolution. "Likewise, although a generation of clinicians has learned that 'normal' systolic blood pressure is approximately 100 mmHg plus age, it is now evident that this is not the physiological norm either."
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