Open AccessImpairment of Endothelium-Dependent Relaxation by Diesel Exhaust Particles in Rat Thoracic Aorta.
Author(s) -
Masahiko Ikeda,
Motohisa Suzuki,
Ken Watarai,
Masaru Sagai,
Takako Tomita
Publication year - 1995
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.68.183
Subject(s) - phenylephrine , sodium nitroprusside , nitric oxide , thoracic aorta , chemistry , acetylcholine , endothelium , aorta , endothelial dysfunction , pharmacology , medicine , anesthesia , endocrinology , blood pressure
Nitric oxide released from vascular endothelium plays important regulatory roles in cardiovascular and pulmonary systems. Epidemiological studies suggest that diesel exhaust particles (DEP) seem to be one of the causative factors responsible for the recent increase in pulmonary diseases. To clarify the pathogenic mechanism, the effects of DEP on vascular endothelial functions were investigated in terms of endothelium-dependent relaxation. Ring preparations of rat thoracic aorta were preincubated for 10 min with a DEP suspension (1, 10, 100 micrograms/ml) at 37 degrees C in organ baths and relaxed with cumulative additions of acetylcholine following precontraction with phenylephrine (10(-6) M). The relaxation was attenuated by DEP-exposure in a concentration-dependent manner. An addition of superoxide dismutase (SOD) completely abolished the inhibitory effect of DEP at lower concentrations, but only partially at the higher concentration. DEP (10 micrograms/ml) neither affected the contractile response to phenylephrine in intact aortic rings nor the endothelium-independent relaxation by sodium nitroprusside in denuded rings, while DEP (100 micrograms/ml) significantly attenuated both responses. These results suggest that 1) inhaled DEP causes pulmonary inflammation by inhibiting the endothelial formation and/or the effect of nitric oxide and 2) SOD reduces the adverse effects.