Exposure to ultrafine carbon particles at levels below detectable @entity55 affects cardiovascular performance in spontaneously @entity101 XXXX .

@entity101 @entity66 @entity55 @entity22456 @entity1003 @entity3449 @entity1827 @entity35 @entity65
BACKGROUND: Exposure to particulate matter is a risk factor for @entity66 but the underlying molecular mechanisms remain poorly understood. In the present study we sought to investigate the cardiopulmonary responses on spontaneously @entity101 @entity35 (SHRs) following inhalation of UfCPs (24 h, 172 mug.m-3), to assess whether compromised animals (SHR) exhibit a different response pattern compared to the previously studied healthy @entity35 (WKY). METHODS: Cardiophysiological response in SHRs was analyzed using radiotelemetry. Blood pressure (BP) and its biomarkers plasma @entity3449 -angiotensin system were also assessed. Lung and cardiac mRNA expressions for markers of oxidative stress ( @entity22456 ), @entity1003 (tissue factor, plasminogen activator inhibitor-1), and endothelial function ( @entity1827 , and endothelin receptors A and B) were analyzed following UfCPs exposure in SHRs. UfCPs-mediated inflammatory responses were assessed from broncho-alveolar-lavage fluid (BALF). RESULTS: Increased BP and heart rate (HR) by about 5% with a lag of 1-3 days were detected in UfCPs exposed SHRs. Inflammatory markers of BALF, lung (pulmonary) and blood (systemic) were not affected. However, mRNA expression of @entity22456 , @entity1827 , endothelin receptors A and B, tissue factor, and plasminogen activator inhibitor showed a significant induction (~2.5-fold; p < 0.05) with @entity1827 being the maximally induced factor (6-fold; p < 0.05) on the third recovery day in the lungs of UfCPs exposed SHRs; while all of these factors - except @entity22456 - were not affected in cardiac tissues. Strikingly, the UfCPs-mediated altered BP is paralleled by the induction of @entity3449 -angiotensin system in plasma. CONCLUSION: Our finding shows that UfCPs exposure at levels which does not induce detectable @entity55 , triggers distinct effects in the lung and also at the systemic level in compromised SHRs. These effects are characterized by increased activity of plasma @entity3449 -angiotensin system and circulating white blood cells together with moderate @entity101 and decreases in heart rate variability. This systemic effect is associated with pulmonary, but not cardiac, mRNA induction of biomarkers reflective of oxidative stress; activation of vasoconstriction, stimulation of @entity1003 factors, and inhibition of fibrinolysis. Thus, UfCPs may cause @entity65 , in the absence of detectable @entity55 , in individuals suffering from preexisting @entity65 .
