Magnesium and blood pressure: A physiology-based approach 81 4 supplements or potassium supplements were followed for 6 months. Nineteen out of the 20 patients showed a significant decrease in BP in the magnesium group, while in the potassium group no significant differences were observed before and after 6 months. In the last decade, clinical trials showed overall small, but clinically relevant effects of magnesium on BP 16,17. Moreover, the total daily dose of magnesium supplementation might be essential, since the meta-analysis of Kass and others reported a more pronounced effect of magnesium supplementation on BP in a subgroup with a higher dose (> 370 mg/d) 16. More recently, a meta-analysis including 34 clinical trials found overall significant BP lowering effects of magnesium 18. Systolic and diastolic BP were significantly reduced (-2.00 and 1.78 mmHg, respectively) at a median dose of 368 mg/d. The effect of magnesium on BP has not only been observed in healthy and hypertensive subjects, but also in subjects with insulin resistance, pre-diabetes and other chronic diseases 19. In these high-risk populations, average systolic and diastolic BP reductions of 4.18 and 2.27 mmHg, respectively, have been noted, which might have clinically relevant effects on cardiovascular health outcomes. Potential mechanisms Although current evidence from both observational and intervention studies suggests beneficial effects of magnesium on BP, the potential underlying mechanisms remain partly unclear. Yet, emerging data from mechanistic studies revealed that magnesium influences several pathways that may improve vascular stiffness, reduce vascular resistance, and lower circulating volume (Figure 1). These beneficial effects on the physiological components of BP, will be addressed in more detail below. Magnesium and cardiac output Previous studies demonstrated effects of magnesium on the cardiac output through inhibiting the renin angiotensin aldosterone system (RAAS), particularly its components angiotensin II and aldosterone. The RAAS plays a fundamental role in the physiology of BP and the pathophysiology of hypertension. It regulates blood volume, vascular resistance, cardiac output, and arterial pressure. Angiotensin II is a key effector hormone of the RAAS. Through promoting sodium retention and vasoconstriction, angiotensin II increases the effective circulating volume and thereby cardiac output. Aldosterone, which is stimulated by angiotensin II, also stimulates reabsorption of fluid and sodium as well as the excretion of potassium 20. Several studies reported inverse relationships between magnesium and aldosterone production 21–25. Atarashi and colleagues found
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