The time course of vasoconstriction and endothelin receptor A expression in pulmonary arterioles of mice continuously exposed to ambient urban levels of air pollution.
The present study aimed to verify the time course of the effects of environmental levels of urban air pollution toxicity on lung arterioles. BALB/c mice (n=56) were continuously exposed to selective chambers equipped with (filtered, F) or without (non-filtered, NF) filter devices for particles and toxic gases for 24h/day, over 14, 21, 30 or 45 days. After exposure, we evaluated the lumen-wall relationship (an estimator of arteriolar narrowing), endothelial nitric oxide synthase (eNOS) and endothelin type A receptor (ETAr) expression in the vascular wall and inflammatory influx of the peribronchiolar area. Concentrations of fine particulate matter (PM<or=2.5 microg/m(3)), nitrogen dioxide (NO(2)), black smoke (BS), humidity and temperature in both the environment and inside the chambers were measured daily. Filters cleared 100% of BS and 97% of PM inside the F chamber. The arteriole wall of the lungs of mice from NF chamber had an increased ETAr expression (p<or=0.042) concomitant to a decrease in the lumen/wall ratio (p=0.02) on the early days of exposure, compared to controls. They also presented a progressive increment of inflammatory influx in the peribronchiolar area during the study (p=0.04) and decrement of the eNOS expression on the 45th day of exposure in both vascular layers (p<or=0.03). We found that after 14 days of exposure, the ambient levels of air pollutants in Sao Paulo induced vasoconstriction that was associated with an increase in ETAr expression. These vascular results do not appear to be coupled to the progressive inflammatory influx in lung tissue, suggesting a down-regulation of vasoconstrictive mechanisms through an imbalance in the cytokines network. It is likely that these responses are protective measures that decrease tissue damage brought about by continuous exposure to air pollutants.
Laboratory of Experimental Air Pollution, Department of Pathology, University of Sao Paulo, Sao Paulo, Brazil.
Giselli
G
Matsumoto
Naomi Kondo
NK
Nakagawa
Rodolfo de Paula
RP
Vieira
Thais
T
Mauad
Luis Fernando Ferraz
LF
da Silva
Carmen Diva Saldiva
CD
de André
Regiani
R
Carvalho-Oliveira
Paulo Hilário Nascimento
PH
Saldiva
Maria Lucia Bueno
ML
Garcia
D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D001160:Arterioles / Q000187:drug effects / Q000378:metabolism; D001273:Atmosphere Exposure Chambers; D002947:Cities; D019570:Inhalation Exposure / Q000032:analysis; D008168:Lung / Q000098:blood supply* / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009585:Nitrogen Dioxide / Q000633:toxicity; D052638:Particulate Matter / Q000633:toxicity; D044022:Receptor, Endothelin A / Q000187:drug effects / Q000378:metabolism*; D012906:Smoke; D013995:Time; D018675:Toxicity Tests; D014661:Vasoconstriction / Q000187:drug effects*
D000393:Air Pollutants; D052638:Particulate Matter; D044022:Receptor, Endothelin A; D012906:Smoke; D009585:Nitrogen Dioxide