The theory that high salt (sodium) intake is the cause of hypertension is controversial. One of the main problems, is that until recently researchers were not fully understanding of the mechanisms by which salt could cause blood pressure changes. Some evidence certainly suggests that increasing salt intake can cause a 2 to 4 mM rise in plasma sodium, and individuals with hypertension have been shown to have a raised plasma levels of sodium. Research has also shown that increased salt intake is associated with blood pressure rises in some individuals, but other research has shown no such association. Low birth weight has been shown to be inversely associated with systolic blood pressure and in low birth weight individuals higher salt intakes (up to 10 g/d) were associated with increased blood pressure. Salt may therefore be positively correlated with blood pressure in some individuals.
Recent evidence supports a role for oxidative stress and vascular dysfunction in the development of hypertension. In healthy endothelial tissue, nitric oxide synthase catalyses the generation of nitric oxide, also called endothelium-derived relaxing factor (EDRF), from the amino acid arginine and molecular oxygen. Nitric oxide is used by the endothelial lining of blood vessels as a signal to cause relaxation of smooth muscle, which when stimulated in the vasculature as a whole, can have blood pressure reducing effect. Oxidative stress is thought to interfere with the production of nitric oxide, which may have implications for increases in blood pressure long-term. High plant intakes (here) and the flavonoid quercetin (here) have been shown to decrease blood pressure possibly because of increased in vivo antioxidant effects. In a similar way to oxidation, salt may interfere with nitric oxide production and lead to increased vasoconstriction and blood pressure increases.
Researchers1 have investigated the effect of small sodium increases on nitric oxide synthase activity in cell models. A 5mM increase in salt concentration from 137 to 142mM caused a 25% decrease in nitric oxide synthase activity in living bovine aortic endothelial cells, with a doses response effect being observed. A similar inhibitory effect of salt on nitric oxide synthase was seen in Chinese hamster ovary cells, but not with a control consisting of mannitol, which suggested the effect was not due to osmosis. Salt also decreased nitric oxide stimulated proliferation of endothelial cells in an ex vivo aortic angiogenesis model. When salt was infused in vivo to rats (increasing plasma salt concentrations by 5 or 20mM), acute rises in blood pressure were detected in a dose response manner. These results support the evidence that salt may interfere with nitric oxide synthase production in endothelial cells.
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