Referenced in: none

Automatically associated channels: Kir2.3

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

Authors: Judy L Aschner, Thuy K Smith, Nora Kovacs, Joaquim M B Pinheiro, Mamta Fuloria

Journal, date & volume: Am. J. Physiol. Lung Cell Mol. Physiol., 2002 Aug , 283, L373-82

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/12114199

Abstract
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.