Relation between tobacco use and urinary excretion of thromboxane A2 and prostacyclin metabolites in young men

Cigarette smoking is a risk factor for cardiovascular disease. The present study addressed the effect of tobacco use on the formation of two eicosanoids, thromboxane A2 and prostacyclin, which have been implicated in both acute and chronic cardiovascular disorders. In 577 randomly sampled 18-19-year...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 1991-05, Vol.83 (5), p.1698-1704
Main Authors: WENNMALM, A, BENTHIN, G, GRANSTROM, E. F, PERSSON, L, PETERSSON, A.-S, WINELL, S
Format: Article
Language:English
Subjects:
6-Ketoprostaglandin F1 alpha - analogs & derivatives
6-Ketoprostaglandin F1 alpha - urine
Adolescent
Adult
Biological and medical sciences
Epoprostenol - metabolism
Humans
Male
Medical sciences
Osmolar Concentration
Smoking
Thromboxane A2 - metabolism
Thromboxane B2 - analogs & derivatives
Thromboxane B2 - urine
Tobacco, tobacco smoking
Toxicology
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Summary:Cigarette smoking is a risk factor for cardiovascular disease. The present study addressed the effect of tobacco use on the formation of two eicosanoids, thromboxane A2 and prostacyclin, which have been implicated in both acute and chronic cardiovascular disorders. In 577 randomly sampled 18-19-year-old men, the urinary excretion of the 2,3-dinor metabolites of thromboxane A2 and prostacyclin (Tx-M and PGI-M, respectively) was analyzed and related to the subjects' self-reported use of tobacco. Sixty-five percent of the subjects used no tobacco, 7.5% were cigarette smokers, 22% used wet (oral) snuff, and the rest reported a mixed use of tobacco. The urinary excretion of Tx-M was higher (p less than 0.001) in cigarette smokers than in those not using tobacco (180 versus 128 pg/mg creatinine) and was correlated (r = 0.35, p less than 0.05) with the daily cigarette consumption. Snuff users had no increase in their urinary excretion of Tx-M, despite urinary cotinine levels comparable to those in the cigarette smokers (1,210 and 1,560 ng/ml, respectively). The excretion of PGI-M did not differ between non-tobacco users, cigarette smokers, and snuff users. We conclude that cigarette smoking, but not the use of snuff, facilitates the formation of thromboxane A2. We propose that such an increased formation reflects platelet activation in the absence of vascular injury and that it may be of significance for the subsequent development of cardiovascular disease.
ISSN:0009-7322
1524-4539
DOI:10.1161/01.cir.83.5.1698