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Published ahead of print on July 8, 2004, doi:10.1165/rcmb.2004-0051OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 5, November 2004, 501-509

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Submitted on February 11, 2004
Revised on July 8, 2004

Cigarette Smoke Induces Persisting Increases of Vasoactive Mediators in Pulmonary Arteries

Joanne L Wright1*, Hsin Tai1, and Andrew Churg1

1 Department of Pathology, University of British Columbia, Vancouver, BC, Canada

* To whom correspondence should be addressed. E-mail: jlwright{at}interchange.ubc.ca.

The pathogenesis of cigarette smoke-induced pulmonary hypertension is not understood. We previously reported that a single smoke exposure acutely but transiently upregulated gene expression of the vasoconstrictor/vasoproliferative agents endothelin (ET), and vascular endothelial growth factor (VEGF) in pulmonary arteries from rat lungs. To determine whether similar changes occurred with chronic smoke exposure we exposed Hartley guinea pigs, an outbred strain that develops pulmonary hypertension, to smoke for 2, 4, or 12 weeks. Small intrapulmonary artery branches were isolated using laser capture microdissection, and gene expression determined by real time PCR. In smoke exposed animals, there were significantly elevated but variable increases in gene expression, with some animals demonstrating 30 to 50 fold increases. Increases in ET and VEGF expression occurred early and persisted through the exposure period, whereas increases in expression of the vasodilator, endothelial nitric oxide synthase (eNOS), developed more slowly. Protein levels of these mediators were also elevated by immunohistochemical staining and correlated with increases in gene expression levels. We conclude that in some animals cigarette smoke induces persisting and marked vascular production of mediators that control vascular muscularization and contraction/dilation. These changes may be important in the development of smoke-induced pulmonary hypertension.




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