Chapter 4 86 recent studies indicate that anti-inflammatory therapy reduces the risk of recurrent cardiovascular events, independently of lipid-lowering, positioning inflammation as a major (actionable) therapeutic target in cardiovascular patients 51. Furthermore, inflammation may increase BP through inhibiting the production of nitric oxide in endothelial cells, causing vasoconstriction. Song and others reported an inverse relationship between markers of inflammation and dietary magnesium intake 52, and suggested that the observed association might partly be explained by a link between magnesium homeostasis and insulin resistance. Hypomagnesaemia may cause insulin resistance 53,54, which is in turn strongly correlated with inflammation and endothelial dysfunction 55. Alternatively,magnesiummay affect insulin sensitivity through modulating inflammation and endothelial function. Insulin Concentrations of intra- and extracellular magnesium are tightly regulated, and the intracellular magnesium appears to be dependent on the extracellular magnesium level. Insulin has been proposed as one of the most important regulatory hormones of magnesium homeostasis, at least in part through an ATPase-dependent pump 54. In vitro studies have shown that, after ingestion of a glucose load, insulin causes a shift from extracellular to intracellular space, resulting in a decrease in circulating magnesium with a simultaneous increase in intra-erythrocyte magnesium 54,56. Once in the cell, magnesium is able to decrease intracellular calcium concentrations, causing vasodilation 54. Conversely, clinical trials have also shown positive effects of magnesium supplementation on insulin resistance 57,58. A recently published epidemiological study reported a positive association of both magnesium intake and status on the risk of diabetes and found that the associationwas partlymediated through insulin resistance 59. This relationship might be explained by actions of intracellular magnesium on tyrosinekinase activity at the insulin receptor level. Although the mechanistic link between insulin resistance and BP regulation remains unclear, it has been suggested that insulin resistance inhibits production of nitric oxide and prostacyclin and induce inflammation 55. Noradrenaline Shimosawa and others found that magnesium inhibits the release of noradrenaline after infusion of magnesium sulfate in spontaneously hypertensive rats and that this effect was mediated by the inhibition of N-type calcium channels in differentiated PC12 cells 60. These findings indicate that magnesium might attenuate sympathetic tone by inhibiting N-type calcium channels. In another study, urinary excretion of noradrenaline
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