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Luminal ATP-induced contraction of rabbit pulmonary arteries and role of purinoceptors in the regulation of pulmonary arterial pressure

Cited 12 time in Web of Science Cited 13 time in Scopus
Authors
Baek, Eun Bok; Yoo, Hae Young; Park, Su Jung; Kim, Hyang Sun; Kim, Seong Deok; Earm, Yung E; Kim, Sung Joan
Issue Date
2008-06-11
Publisher
Springer Verlag
Citation
Pflugers Arch. 457(2):281-291
Keywords
Adenosine Triphosphate/analogs & derivatives/*metabolism/pharmacologyAnimalsAnoxia/metabolism/physiopathology*Blood PressureCalcium Signaling*Coronary Circulation/drug effectsCoronary Vessels/drug effects/*metabolismEndothelium, Vascular/metabolismFemaleMaleMembrane PotentialsMuscle, Smooth, Vascular/metabolismPatch-Clamp TechniquesPerfusionPulmonary Artery/drug effects/*metabolism/physiopathology*Pulmonary Circulation/drug effectsRabbitsReceptors, Purinergic P2/drug effects/*metabolismRespiration, ArtificialSpectrometry, FluorescenceSuramin/pharmacologyUridine Triphosphate/metabolism*Vasoconstriction/drug effectsVasodilationVideo Recording
Abstract
The effects of luminal ATP between rabbit pulmonary (PAs) and coronary arteries (CAs) were compared to understand the role of purinoceptors in the regulation of pulmonary arterial pressure (PAP) under hypoxia. Diameters of vessels were video analyzed under luminal perfusion. ATP-induced membrane currents and intracellular Ca(2+) signals ([Ca(2+)](i)) were compared in pulmonary (PASMCs) and coronary myocytes (CASMCs) using patch clamp and spectrofluorimetry. PAP was measured in perfused lungs under ventilation. Luminal ATP induced constriction of rabbit PAs in the presence of endothelium. In contrast, CAs showed dilating responses to luminal ATP even in the absence of endothelium. In PASMCs, both P2X-mediated inward current and P2Y-mediated store Ca(2+) release were consistently observed. In contrast, CASMCs showed neither P2X nor P2Y responses. In the perfused lungs, hypoxia-induced PAP increase was decreased by suramin, a purinergic antagonist. A luminal application of alpha,beta-meATP largely increased PAP, whereas UTP decreased PAP. The combined application of P2X- and P2Y-selective agonists (alpha,beta-meATP and UTP) increased PAP. However, the perfusion of ATP alone decreased PAP, and the ATP-induced PAP decrease was affected neither by adenosine receptor antagonist nor by nitric oxide synthase inhibitor. In summary, although the luminal ATP constricts isolated PAs and suramin attenuated the HPV of perfused lungs, the bimodal responses of PAP to purinergic agonists indicate that the luminal ATP regulates pulmonary circulation via complex signaling interactions in situ.
ISSN
0031-6768 (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18542991

http://www.springerlink.com/content/c8370761560p63j3/fulltext.pdf

http://hdl.handle.net/10371/68110
DOI
https://doi.org/10.1007/s00424-008-0536-z
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College of Medicine/School of Medicine (의과대학/대학원)Dept. of Physiology (생리학교실)Journal Papers (저널논문_생리학교실)
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