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Simulated sleep apnea augments endothelin activation by diesel exhaust exposure

Some individuals experience acute cardiovascular events following exposure to air pollutants that are triggered by vasospasm. Because the pollutant diesel exhaust (DE) increases endothelin (ET) synthesis and sympathetic nervous system activity (SNSA), these events may be key to DE‐induced cardiovascular sequelae. Sleep apnea patients and rats exposed to intermittent hypoxia/hypercapnia (IH/HC) to mimic sleep apnea have elevated SNSA and augmented vascular responses to ET. We hypothesized that IH/HC rats would respond to DE with greater ET synthesis and augmented SNSA compared to air‐exposed rats. Rats treated with IH/HC or air for 14 days were exposed to 5 hrs of DE (300 μg/m3) or air. Arterial pressure (AP), electrocardiograms (ECG) and heart rate (HR) were recorded using telemetry. Tissues were obtained after DE exposure to measure ET‐1 mRNA. HR variability as an index of SNSA was derived from ECG (ratio of low to high frequency of transformed RR interval). Although DE elevated AP in both groups compared to air exposed groups, AP tended to be higher in DE IH/HC rats (p<0.05). DE increased ET‐1 mRNA in hearts and coronary arteries only in IH/HC rats (p<0.05) and increased SNSA in both groups. The DE exposure‐induced increase in ET‐1 message with SNS activation suggests these variables may play an important role in mediating detrimental vascular effects of DE in IH/HC rats and contribute to exacerbated responses to DE in sleep apnea patients.