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Am J Physiol Lung Cell Mol Physiol (March 22, 2002). doi:10.1152/ajplung.00032.2002
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Articles in PresS, published online ahead of print March 22, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00032.2002
Submitted on January 22, 2002
Accepted on March 18, 2002

Mechanisms of bradykinin-mediated dilation in newborn piglet pulmonary conducting and resistance vessels

Judy L. Aschner1*, Thuy K. Smith1, Nora Kovacs1, Joaquim M. B. Pinheiro2, and Mamta Fuloria1

1 Pediatrics, Wake Forest University School of Medicine, Winston-Salem, NC, USA
2 Pediatrics, Albany Medical College, Albany, NY, USA

* To whom correspondence should be addressed. E-mail: jaschner{at}wfubmc.edu.

Bradykinin (BK) is a potent dilator of the perinatal pulmonary circulation. We investigated segmental differences in BK-induced dilation in newborn pig large conducting pulmonary artery and vein rings and in pressurized pulmonary resistance arteries (PRA). In conducting pulmonary arteries and veins, BK-induced relaxation is abolished by endothelial disruption and by inhibition of nitric oxide synthase (NOS) with nitro-L-arginine (L-NA). In PRA, two-thirds of the dilation response is L-NA-insensitive. Charybdotoxin plus apamin and depolarization with KCl abolish the L-NA-insensitive dilations, findings that implicate the release of endothelial-derived hyperpolarizing factor (EDHF). However, endothelial-disrupted PRA retain the ability to dilate to BK, but not to ACh or A23187. In endothelial-disrupted PRA, dilation was inhibited by charybdotoxin. Thus in PRA, BK elicits dilation by multiple and duplicative signaling pathways. Release of NO and EDHF contribute to the response in endothelium-intact PRA; in endothelial-disrupted PRA, dilation occurs by direct activation of vascular smooth muscle K-Ca channels. Redundant signaling pathways mediating pulmonary dilation to BK may be required to assure a smooth transition to extrauterine life.




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