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Am J Physiol Lung Cell Mol Physiol 283: L373-L382, 2002. First published March 22, 2002; doi:10.1152/ajplung.00032.2002
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Vol. 283, Issue 2, L373-L382, August 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 Department of Pediatrics, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1081; and 2 Department of Pediatrics, Albany Medical College, Albany, New York 12208

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 (NO) synthase 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 endothelium-derived hyperpolarizing factor (EDHF). However, endothelium-disrupted PRA retain the ability to dilate to BK but not to ACh or A-23187. In endothelium-disrupted PRA, dilation was inhibited by charybdotoxin. Thus in PRA, BK elicits dilation by multiple and duplicative signaling pathways. Release of NO and EDHF contributes to the response in endothelium-intact PRA; in endothelium-disrupted PRA, dilation occurs by direct activation of vascular smooth muscle calcium-dependent potassium channels. Redundant signaling pathways mediating pulmonary dilation to BK may be required to assure a smooth transition to extrauterine life.

pulmonary resistance arteries; endothelium; nitric oxide; calcium-dependent potassium channels; endothelium-derived hyperpolarizing factor


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