The current literature is inconclusive with respect to these findings. Numerous studies have confirmed a link between high dietary sodium intake and blood pressure.
3,
4,
5,
7 This link is traditionally explained by the Guyton Hypothesis, whereby increased sodium intake promotes increased blood pressure via extracellular fluid volume expansion.
8 More recent literature also supports a key role of the vasculature to elevate blood pressure in response to sodium intake, independent of renal sodium excretion.
9 With regard to calcium, the literature is controversial. Some research supports that high urinary calcium excretion is associated with elevated blood pressure.
10,
11 Other evidence suggests that diets supplemented with calcium mildly reduce blood pressure, with a possible dose–response effect.
12 It should also be noted that high dietary calcium consumption may increase cardiovascular risk via promotion of arterial calcification.
13 The role of magnesium in blood pressure control is less clear. However, magnesium supplementation has been used to prevent eclampsia.
14 Although not completely characterized, magnesium likely acts as a vasodilator to reduce peripheral vascular resistance or to relieve vasoconstriction.
15