Magnesium homeostasis in cardiorespiratory comorbidity: shared pathogenetic mechanisms and therapeutic potential in COPD and arterial hypertension

Abstract

Chronic obstructive pulmonary disease (COPD) and arterial hypertension are characterised by a high level of comorbidity, based on systemic inflammation and oxidative stress. Magnesium deficiency significantly intensifies these pathological processes; however, traditional serum markers often do not reflect true tissue depletion.

Objective. To summarise the role of magnesium deficiency in the pathogenesis of COPD and essential hypertension, identify common molecular targets, and assess the clinical potential of systemic and local (nebulised) therapy.

Results. Magnesium deficiency acts as a powerful catalyst of mitochondrial and endothelial dysfunction, sustaining neutrophilic inflammation in the lungs and calcium-dependent constriction in the vessels. Despite the fundamental consistency of these effects, the practical use of oral magnesium supplementation remains controversial because of the diagnostic limitations of serum magnesium. At the same time, local delivery (nebulised magnesium sulfate) demonstrates a favourable safety profile and a selective pulmonary effect without systemic hypotension.

Conclusions. Correction of magnesium metabolism is promising but requires improved diagnostic criteria and optimisation of routes of administration for patients with cardiorespiratory comorbidity.