Altura · Mineral and electrolyte metabolism 1993 · narrative review · n=?

Magnesium, hypertensive vascular diseases, atherogenesis, subcellular compartmentation of Ca2+ and Mg2+ and vascular contractility.

Cited 88 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Narrative review and mechanistic evaluation without systematic synthesis or primary human trial data

PubMed 8264520 · record verified 2026-08-29

What was done

This narrative review synthesized experimental, epidemiological, and clinical evidence regarding dietary magnesium deficiency and altered magnesium metabolism in ischemic heart disease, hypertension, diabetic vascular disease, atherosclerosis, and vasospasm. It detailed laboratory observations using digital imaging microscopy with molecular fluorescent probes and ion-selective electrodes to evaluate extracellular and intracellular ionized magnesium and calcium dynamics in vascular smooth muscle and endothelial cells.

What was found

The abstract reports qualitative mechanistic findings without numeric values or effect sizes. Extracellular ionized magnesium ([Mg2+]o) regulates divalent cation transport, intracellular release, and subcellular compartmentation of free calcium ([Ca2+]i) and free magnesium ([Mg2+]i) in vascular smooth muscle and endothelial cells. Measurements with ion-selective electrodes revealed that extracellular ionized magnesium levels fluctuate more rapidly in cardiovascular pathophysiological states than previously recognized, thereby functioning as a key determinant of vascular tone and reactivity.

Why it matters

The paper outlines subcellular and physiological mechanisms by which ionized magnesium influences vascular smooth muscle contraction and endothelial cell function. It provides biological plausibility for epidemiological links between magnesium deficiency and cardiovascular pathology.

Limits

The abstract provides no quantitative data, sample sizes, or formal systematic search criteria. As a narrative synthesis centered on bench-level and cellular physiology, it cannot establish clinical outcomes or therapeutic thresholds in human populations.

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