Role for trpa1 in diesel-induced arrhythmia risk.
Diesel exhaust (DE) is a complex mixture of toxic gaseous and particulate components associated with adverse cardiovascular effects such as arrhythmias. Hazari et al. (p. 951) hypothesized that increased risk of triggered arrhythmias 1 day after DE exposure would be mediated by airway sensory nerves bearing transient receptor potential (TRP) channels that, when activated by noxious chemicals, cause a centrally mediated autonomic imbalance and heightened risk of arrhythmia. Spontaneously hypertensive rats implanted with radiotelemeters were exposed to whole DE (wDE), filtered DE (fDE), or filtered air (controls) for 4 hr. Arrhythmogenesis was assessed 24 hr later by continuous intravenous infusion of aconitine, an arrhythmogenic drug, while heart rate and electrocardiogram were monitored. Animals exposed to DE had increased sympathetic modulation, prolonged ventricular depolarization, and shortened repolarization periods, and they developed arrhythmia at lower doses of aconitine than controls. Pretreatment with a TRPA1 antagonist or sympathetic blockade prevented the heightened sensitivity to arrhythmia. Gaseous components appear to play an important role in the proarrhythmic response to DE, which may be mediated by activation of TRPs. These results provide a biological basis for the association between exposure to air pollutants and arrhythmias.
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|Publication:||Environmental Health Perspectives|
|Article Type:||Brief article|
|Date:||Jul 1, 2011|
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