The effect of particulate matter on resistance and conductance vessels in the rat.
Epidemiological and clinical studies suggest that air pollution, in particular ambient particulate matter (PM), increases mortality in patients with cardiovascular disease (CVD). Several in vivo studies have shown an increase of blood pressure by PM, but so far the mechanism or responsible particle-component has not been elucidated. We exposed small mesenteric rat artery (SMRA) and rat aorta to ambient particles (EHC-93) to test the ability of ambient particles to modify the vascular tone of different vessel types. PM suspensions (10-100 microg/ml) and filtrates containing only the water-soluble components failed to modify the resting tension of either the aorta or SMRA. However, PM did elicit a dose-dependent vasorelaxation in phenylephrine precontracted SMRA and aorta. The effect of the PM suspensions was higher than that of PM filtrate (without particles). The relaxation was already visible at 10 microg/ml, and the difference with filtrate became significant at 100 microg/ml for aorta (maximal relaxation E(max) = 18% vs. 12% PM filtrate) and as low as 30 microg/ml for SMRA (E(max) = 13% vs. 5% PM filtrate). Although the effect of PM was biggest in aorta, the concentration to cause half of the maximal effect (EC(50)) of suspension and filtrate was the same in both capacity (aorta) and resistance vessels (SMRA). The main difference seen between SMRA and aorta was that PM did not modify the phenylephrine-induced dose-response vasoconstriction in SMRA, while it did do so in the aorta. In conclusion, the in vitro exposure of precontracted blood vessels to ambient PM results in an acute vasorelaxation, which is in contrast to the observation that PM can cause increased blood pressure. Dose calculations show that the elevation of blood pressure observed in vivo is not likely due to direct effects of particles or constituents. We therefore suggest that the in vivo effect of PM on vasoconstriction acts through other pathways, such as the central nervous system.
Bagaté
Karim
K
Particle Research, Institut fur Umweltmedizinische Forschung, University of Düsseldorf, Duesseldorf, Germany. Karim.bagate@uni-duesseldorf.de
Meiring
James J
JJ
Cassee
Flemming R
FR
Borm
Paul J A
PJ
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000502:physiology; D019327:Copper Sulfate / Q000633:toxicity; D004305:Dose-Response Relationship, Drug; D066298:In Vitro Techniques; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects / Q000502:physiology; D010316:Particle Size; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D011921:Rats, Inbred WKY; D014655:Vascular Resistance / Q000187:drug effects*; D014661:Vasoconstriction / Q000187:drug effects*; D014664:Vasodilation / Q000187:drug effects*; D019287:Zinc Sulfate / Q000633:toxicity
D000316:Adrenergic alpha-Agonists; D000393:Air Pollutants; D010656:Phenylephrine; D019287:Zinc Sulfate; D019327:Copper Sulfate