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4252568 
Journal Article 
Abstract 
Role of transient receptor potential (TRP) channels in ozone-induced decreases in blood pressure and heart rate in rats on a high fructose diet 
Wagner, JG; Allen, K; Nan, B; Lewandowski, R; Fink, G; Harkema, JR, JR 
2013 
Yes 
American Journal of Respiratory and Critical Care Medicine
ISSN: 1073-449X
EISSN: 1535-4970 
187 
A5093 
English 
WOS:000209838401727 
Rationale: People with diet-induced cardiometabolic disorders (diabetes, hypertension) may be more susceptible to the adverse cardiopulmonary effects of air pollution exposures. We have previously demonstrated that ozone-induced decreases in heart rate and blood pressure are exacerbated in a rat model of the cardiometabolic syndrome. Activation of airway irritant receptors such as transient receptor potential channels (TRP) by ozone can mediate pulmonary responses, but their role in cardiovascular regulation by ozone is unknown.

Methods: Male Sprague Dawley rats were fed a high-fructose diet for eight weeks and then exposed to filtered air (FA) or ozone (O3; 0.5ppm) for 5 hours. Thirty minutes before the start of exposure rats were treated with Ruthenium Red (RR) a non-selective TRPV channel antagonist, or HC-030031 (HC) a selective antagonist of TRPA1 activation, or vehicle, i.p. Heart rate (HR), body temperature, mean arterial (MAP) and systolic blood pressure (SBP) were collected by radiotelemetry every 5 minutes during the exposure, and for three hours immediately after exposure.

Results: During ozone exposure, decreases in HR (30 bpm), MAP (10 mmHg), SBP (11 mmHg) and body temperature (1oC) were measured in vehicle-treated rats. Temperature returned to normal shortly after the end of exposure. By comparison, exposure-related effects on HR and blood pressure persisted during the post exposure period, albeit to lesser degrees than that observed during the exposure. Pretreatment with HC had no effect on ozone-induced responses during exposure. However, in RR- treated rats, ozone did not cause decreases in temperature and SBP, and exposure-related effects on MAP were partially reduced. During the post-exposure period, neither TRP channel antagonist altered the persistence of ozone-induced changes in HR and MAP.

Conclusions: Cardiovascular responses to ozone in the face of cardiometabolic syndrome are independent of TRPA1 pathways. The involvement of TRPV channels in modulating ozone-induced cardiovascular responses requires further study. Funded by US EPA RD83479701. 
American Thoracic Society 2013 International Conference 
Philadelphia, PA 
May 17-22, 2013