In asthmatics, nocturnal asthma (nighttime asthma) can make their sleep impossible, leaving them feeling tired and irritable during the day. It also affects their overall quality of life.
Nocturnal asthma is responsible for more than 50% of deaths, revealing an association between nocturnal asthma symptoms and asthma deaths; however, the precise mechanism is unclear.
Now, a study led by Prof. Kentaro Mizuta from Tohoku University Graduate School of Dentistry, Japan, has discovered that the sleep hormone melatonin worsens asthma, according to Science Daily.
People with a history of asthmatic experience bronchoconstriction – the contraction of the smooth muscles of the bronchus. The bronchus is the pathway that moves air to and from the lungs. And to get rid of bronchoconstriction, doctors advise bronchodilators – the medicines that widen the bronchus.
Melatonin is often prescribed to people with insomnia, as it acts as a sleep hormone. However, melatonin favors a state of bronchoconstriction and weakens the relaxing effect of bronchodilators, according to Science Daily. The sleep hormone weakest the effect of bronchodilators by activating the melatonin MT2 receptor.
Prof. Mizuta and team identified the expression of the melatonin MT2 receptor in human airway smooth muscle.
The researchers observed that the activation of the melatonin MT2 receptor using melatonin greatly potentiated bronchoconstriction. Also, they found that melatonin weakened the relaxing effects of a bronchodilator called beta-adrenergic agonist or beta-agonist.
Prof. Mizuta explained, “Although serum concentration of melatonin did not significantly induce the airway constriction, greater doses of melatonin, which is clinically used to treat insomnia, jet lag, or cancer, worsened asthma symptoms and impaired the therapeutic effect of bronchodilators.”
The study’s first author Haruka Sasaki said, “The pharmacological therapy that blocks the melatonin MT2 receptor could inhibit the detrimental effects of melatonin on airways.” The study was published last month in the American Journal of Physiology Lung Cellular and Molecular Physiology.
