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This Article Full Text Full Text (PDF) All Versions of this Article: 285/2/H727    most recent 00269.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Tsakadze, N. L. Articles by D'Souza, S. E. Search for Related Content PubMed PubMed Citation Articles by Tsakadze, N. L. Articles by D'Souza, S. E.

Acrolein-induced vasomotor responses of rat aorta

¹Department of Physiology and Biophysics, ²Division of Cardiology/Department of Medicine, University of Louisville, Louisville, Kentucky 40292

Submitted 25 March 2003 ; accepted in final form 28 April 2003

Acrolein is a highly reactive aldehyde pollutant and an endogenous product of lipid peroxidation. Increased generation of, or exposures to, acrolein incites pulmonary and vascular injury. The effects of acrolein on the vasomotor responses of rat aortic rings were studied to understand its mechanism of action. Incubation with acrolein (10–100 µM) alone did not affect the resting tone of aortic vessels; however, a dose-dependent relaxation of phenylephrine-precontracted aortic rings was observed. Acrolein-induced relaxation was slow and time dependent and the extent of relaxation after 100 min of application was 44.7 ± 4.1% (10 µM), 56.0 ± 5.6% (20 µM), 61.0 ± 7.9% (40 µM), and 96.1 ± 2.1 (80 µM), respectively, versus 14.2 ± 3.3% relaxation in the absence of acrolein. Acrolein-induced vasorelaxation was prevented by endothelial denudation and was abolished on pretreatment with the nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester, the guanylyl cyclase inhibitor 1H-[1,2,4]oxidazolo[4,3-a]quinoxaline-1-one, or the cyclooxygenase inhibitor indomethacin. Inhibition of K⁺ channels (by tetrabutylammonium) or Na⁺-K⁺-ATPase (by ouabain) did not significantly prevent acrolein-mediated vasorelaxation. Exposure to acrolein in the presence or absence of other compounds elicited slow wave vasomotor effect in 77% of aortic vessels versus 1.4% in control. Vasomotor responses were also studied on aortic rings prepared from rats fed 2 mg · kg^–1 · day^–1 acrolein for 3 alternate days by oral gavage. These vessels developed a significantly lower contractile response to phenylephrine compared with controls. Together, these results indicate that acute acrolein exposure evokes delayed vasorelaxation due to a nitric oxide- and prostacyclin-dependent mechanism, whereas in vivo acrolein exposure compromises vessel contractility.

rat aortic rings; vasoreactivity; aldehydes; nitric oxide

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