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1 Pediatrics, University of Toronto, Toronto, Ontario, Canada
* To whom correspondence should be addressed. E-mail: Jaques.Belik{at}sickkids.ca.
The factors accounting for the maintenance of a low pulmonary vascular resistance (PVR) postnatally are not completely understood. The aim of this study was to test the hypothesis that bronchial epithelium produces a factor capable of relaxing adjacent pulmonary arterial smooth muscle. We studied 4th generation intralobar pulmonary arteries and bronchi of 4-8 day-old rats. Arteries were mounted on a wire myograph, alone or with the adjacent bronchus. The presence of the attached bronchus significantly reduced pulmonary artery force generation induced by the thromboxane analogue (U46619) or KCl whether the endothelium was present or absent (P<0.01). The converse was not true in that bronchial force generation was not affected when studied with the adjacent pulmonary artery. Mechanical removal of the bronchial epithelium or addition of the nitric oxide (NO) synthase (NOS) non-specific (L-NMMA) or the specific neuronal NOS (7-nitroindazole) inhibitors increased arterial force generation to levels comparable to the isolated artery preparation. Wortmannin, a phosphatidylinositol 3-kinase (PI3-kinase) inhibitor, significantly decreased (P<0.01) NO release of pulmonary arteries only when the adjacent bronchus was present. We conclude that bronchial epithelium in the newborn rat produces a factor capable of lowering pulmonary vascular muscle tone. This relaxant effect can be suppressed by NOS and PI-3 kinase inhibition suggesting an action via NOS phosphorylation and NO release. We speculate that such a mechanism may be operative in vivo and play an important role in control of PVR in the early postnatal period.
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