Magnesium as a relaxing factor of airway smooth muscles
in the search for effective treatment of a life-threatening asthma attack, intravenous magnesium infusion has been studied in asthmatic patients because of its potential effect to reverse bronchospasm and improve pulmonary function. To determine whether magnesium sulfate inhibits airway smooth muscle contraction and the possible mechanism of its action, in vitro experiments were performed on rabbit tracheas. Tracheal muscle strips were obtained from 12 rabbits. Initially, the muscle strip was pretreated with a solution containing MgSO4 (concentrations 10(-4) to 2 M) and 85 mM KCl. The response curve of the muscle was recorded. Application of the above solution led to a 40% relaxation at a magnesium concentration of 10(-1) M. The time to peak and to wash-out remained unchanged, and fixed to 66.6 and 123.3 sec, respectively, not influenced by magnesium concentration. On a second phase, the muscle strip was pretreated with KCI alone, and only after a full contractile response was obtained did we add 10(-1) M MgSO4, which led to full relaxation. We follow the same protocol using 10(-4) M acetylcholine (ACH). In this case, simultaneous application of 10(-1) M MgSO4 caused a 55.1% decrease in muscle contraction and a 60% decrease in time to peak. On a second phase, we added magnesium as we did with KCI, but without the same result. Magnesium caused a full relaxation when the constrictor agent was KCI, but a residual contraction was observed when the constrictor was ACH. Based on the knowledge that ACH and KCI cause Ca2+ influx into the cells and subsequent contraction by acting on different Ca2+ channels, we concluded that magnesium inhibits Ca2+ influx by blocking the voltage-dependent calcium channels.